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THE    DIAGNOSIS 

OF 

NERVOUS    DISEASES 


PURVES  STEWART,  M.A.,  M.D.  Edin.,  F.R.C.P. 

FHYSICIAN    TO    THE    WESTMINSTER    HOSPITAL  ;     JOINT-LECTURER    ON     MEDICINE    IN 

THE    MEDICAL    SCHOOL  ;     PHYSICIAN    TO    THE    WEST    END    HOSPITAL    FOR 

NERVOUS    DISEASES  ;    MEMBRE    CORRESPONDANT    DE    LA    S0CI£t6 

DE     NEUROLOGIE     DE     PARIS  ;     CORRESPONDING    MEMBER 

OF    THE   PHILADELPHIA    NEUROLOGICAL   SOCIETY  ; 

CONSULTING   PHYSICIAN  TO  H.M.    FORCES  ; 

TEMPORARY   COLONEL   A. M.S. 


FOURTH  EDITION,   REVISED  AND  ENLARGED 


NEW    YORK 
E.    B.    TREAT    &    CO. 

LONDON:   EDWARD   ARNOLD 
1916 

[All  rights  reserved] 


Printed  in  Great  Britain 


PREFACE    TO    THE    FOURTH    EDITION 

This  work  makes  no  pretension  to  rival  or  replace  the  numer- 
ous excellent  text-books  which  are  available  to  the  student. 
Its  function  is  to  supplement  the  more  didactic  treatises 
by  discussing  groups  of  symptoms  as  met  with  in  every-day 
practice. 

The  present  edition  differs  considerably  from  its  pre- 
decessors. Up  till  the  time  of  the  war,  neurology,  like  other 
branches  of  science,  was  making  steady  progress  in  many 
directions.  The  various  advances  necessitated  the  re- writing 
of  a  considerable  proportion  of  the  book,  e.g.  the  parts  dealing 
with  cerebellar  lesions,  the  neuroses,  the  vegetative  nervous 
system,  &c. 

Since  the  war,  however,  life  for  everyone,  in  Europe  at 
least,  has  become  profoundly  changed.  Even  the  present 
volume  exemplifies  this  fact.  Like  many  others  of  my 
profession,  it  has  been  my  privilege  to  be  called  abroad  on 
foreign  service.  For  the  last  year,  attached  as  consulting 
physician  to  his  Majesty's  forces  in  the  Mediterranean,  I  have 
helped,  both  in  hospital  and  in  the  field,  to  watch  the  most 
gallant  patient  in  the  world — the  British  soldier.  Some 
observations  on  organic  war-injuries  have  formed  the  basis 
of  an  additional  chapter.  For  permission  to  publish  them, 
I  am  indebted  to  the  courtesy  of  the  Director-General,  Sir 
Alfred  Keogh. 

Critics  of  the  present  work  will,  I  hope,  make  due  allow- 
ance for  the  geographical  and  other  difficulties  under  which 
it  has  been  produced.  I  am  conscious  of  its  many  short- 
comings. Of  these,  some,  perhaps,  are  due  to  the  absence 
of  facilities   for   reference    to   the   works  of  other  observers. 


iv  PREFACE 

The  personal  character  of  the  observations,  on  the  other  hand, 
may  present  certain  compensating  advantages. 

To  my  fellow-officers,  notably  to  Col.  C.  A.  Ballance  and 
Col.  Charters  Symonds,  my  warmest  thanks  are  due  for  their 
unfailing  courtesy  in  affording  me  opportunities  for  observing 
cases  of  interest  in  numerous  hospitals.  Most  of  all,  I  have 
to  thank  my  friend  Col.  A.  E.  Garrod  for  his  invaluable 
advice,  encouragement,  and  help,  not  only  in  the  correction  of 
the  proof-sheets  but  also  in  the  laborious  preparation  of  the 
index. 

PURVES  STEWART. 

Malta,  April  1916. 


CONTENTS 


OHAP. 

I.  Anatomy  and  Physiology 
II.  Anatomy  and  Physiology  {continued)    . 

III.  Method  of  Case-Taking 

IV.  Coma 

V.  Fits  and  other  Convulsive  Phenomena 

VI.  Involuntary  Movements 

VII.  Aphasia 

VIII.  Disorders  op  Articulation  . 

IX,  Cranial  Nerves 

X.  Cranial  Nerves  {continued)    . 
XI.  Pain  and  other  Abnormal  Subjective  Sensations 
XII.  Abnormalities     of     Sensation  :    Hyperesthesia, 
esthesia,  Anesthesia 

XIII.  Organic  Motor  Paralysis  op  Upper  Neurone  Type 

XIV.  Organic  Motor  Paralysis  of  Lower  Neurone  Type 
XV.  Recurrent  and  Transient  Palsies     . 

XVI.  Inco-ordination 

XVII.  Postures  and  Gaits 

XVIII.  Tropho-Neuroses 

XIX.  Reflexes 

XX.  Affections  of  the  Vegetative  Nervous  System 

XXI.  The  Neuroses 

XXII.  Electro-Diagnosis  and  Electro-Prognosis 

XXIII.  The  Cerebro-Spinal  Fluid 

XXIV.  Disorders  op  Sleep 

XXV.  Intra-Cranial  Tumours 

XXVI.  Organic  War-Lesions  of  the  Nervous  System 


Par- 


PAQE 
1 

34 

55 

62 

74 

88 

106 

119 

128 

157 

181 

198 
215 
232 
260 
269 
280 
304 
330 
351 
378 
415 
429 
451 
462 
487 


INDEX 


559 


PLATES 

I.  Coloured  model  showing  cutaneous  root-areas 
II.  Sub-ungual  haemorrhages  of  the  hand   . 
III.  Erythromelalgia       ...... 


9  face  page 

44 

?)                 )5 

318 

"                 » 

372 

THE    DIAGNOSIS    OF    NERVOUS 
DISEASES 

CHAPTER   I 

ANATOMY    AND    PHYSIOLOGY 

There  is  no  department  of  medicine  in  which  an  accm^ate  know- 
ledge of  anatomy  is  of  greater  importance  than  in  the  diagnosis  of 
nervous  diseases.  Let  us  therefore,  at  the  outset,  recall  some  of 
the  main  points  in  the  anatomy  and  physiology  of  the  nervous 
system. 

The  nervous  system  consists  of  two  main  divisions  : — (1)  the 
cerebro-spinal,  comprising  the  brain  and  spinal  cord,  together 
with  the  cranial  and  spinal  nerves,  and  (2)  the  sympathetic, 
constituted  by  two  chains  of  pre-vertebral  ganglia,  one  on  each 
side  of  the  spine.  These  two,  the  cerebro-spinal  and  sympathetic, 
intercommunicate . 

For  teaching  purposes  it  is  convenient  to  regard  the  nervous 
system  as  built  up  of  nerve -cells,  and  their  processes  the  nerve- 
fibres.  Both  are  excitable.  But  whereas  the  nerve-cell  has 
been  commonly  assumed  to  originate  impulses  as  does  the 
cell  of  an  electric  battery,  the  nerve-fibres  serving  merely  as 
conductors,  it  is  unusual  for  an  impulse  to  arise  within  a 
nerve-cell,  except  as  the  result  of  a  transmitted  impulse.^  Each 
nerve-fibre  is  made  up  of  a  bundle  of  extremely  fine  neuro- 
fibrillse  which  traverse  the  nerve-cell,  entering  it  through  one  process 
and  leaving  it  through  another.  In  this  way  the  nerve-cell  acts 
as  a  convenient  shunt  for  impulses,  receiving  them  from  one 
quarter  and  transmitting  them  to  another.  The  nerve-cell  also 
exerts  a  trophic  influence  over  the  nerve-fibre  and  is  intimately 

1  The  cardiac  and  respiratory  nuclei  in  the  medulla  are  exceptions  to  this 
rule.  These  automatic  centres  can  be  stimulated,  not  only  by  transmitted 
nerve-impulses,  but  also  by  chemical  changes  in  the  blood,  e.g.  by  deficiency 
of  oxygen  and  excess  of  COg  or  of  lactic  acid. 

A 


2  NERVOUS    DISEASES 

concerned  witli  its  nutrition,  so  that  the  nerve-fibre  degenerates 
if  separated  from  its  trophic  nerve-cell. 

In  a  reflex  motor  act,  which  is  the  simplest  manifestation  of 
nervous  energy,  as  for  example  in  the  plantar  reflex,  the  impulse 
or  stimulus  starts  from  a  sensory  end-organ,  in  this  instance  the 
skin  of  the  sole.  The  impulse  travels  up  a  sensory  nerve-fibre, 
through  the  corresponding  posterior  nerve-root  into  the  spinal 
cord,  where,  after  traversing  an  inter-communicating  nerve-fibre 
and  cell  in  the  grey  matter  of  the  cord,  it  reaches  an  anterior 
cornual  cell.  From  this  motor-cell  an  efferent  impulse  starts, 
travels  outwards  along  an  anterior  nerve-root  into   a   peripheral 


Skzjz 


Fig.  1. — Diagram  of  a  Simple  Spinal  Reflex. 

nerve  and  thus  reaches  the  flexor  muscles  of  the  toes  innervated 
by  the  same  segment  of  the  spinal  cord.  The  toe-flexors  promptly 
give  a  single  contraction. 

The  accompanying  diagram  (Fig.  1)  will  serve  to  recall  the  chief 
components  of  a  simple  spinal  reflex,  such  as  we  have  just  described. 

Some  reflexes  occur  unconsciously,  as  for  example  the  reflex 
contraction  of  the  pupil  when  the  retina  is  stimulated  by  light, 
or  again,  the  normal  movements  of  the  stomach  and  intestines. 
But  in  other  cases  the  afferent  impulse,  besides  exciting  a  reflex 
motor  action,  sends  part  of  its  impulse  upwards  to  the  higher 
centres  of  the  opposite  cerebral  cortex,  where  it  produces  a  con- 
scious sensation.  This  is  accomplished  by  means  of  a  sensory  fibre 
passing  upwards  in  the  substance  of  the  spinal  cord  (as  indicated 
in  the  other  diagram — ^Fig.  2),  through  relays  of  nerve-cells  and 


ANATOMY    AND    PHYSIOLOGY 


3 


fibres  in  the  medulla,  pons,  and  so  on,  to  the  perceiving  centre  in 
the  cortex. 

Moreover,  a  discharge  of  motor  energy  from  the  motor  cell  in 
the  anterior  cornu  can  be  produced  not  only  reflexly,  from  below, 
but  also  voluntarily,  from  above.  This  is  achieved  by  an  impulse 
descending  from  the  cortical  motor  centre  of  the  opposite  side, 
through  the  crossed  pyramidal  tract  down  the  cord  to  the  anterior 


Ascending 

Saisory  f 
fibref     ' 


Volurvtary 
Motx?r 
fibre 


Skiro 


Muscle 

Fig.  2. — Diagram  of  a  Voluntary  Motor  Act. 

cornual  cell   (see  Fig.  2).     A   discharge  can   also  be  voluntarily 
inhibited  from  above. 

Confining  ourselves  now  to  the  consideration  of  a  cerebro-spinal 
reflex  motor  action,  we  must  bear  in  mind  that  afferent  impulses, 
on  reaching  the  cortical  sensory  centres,  do  not  necessarily  produce 
a  descending  impulse  along  the  pyramidal  tract.  If  they  do,  this 
is  simply  an  automatic  action,  a  reflex  of  longer  path.  There 
exist  in  the  cortex  perceiving-centres  which  take  cognisance  of  the 
source  and  nature  of  the  stimulus,  and  determine  whether  or  no 
any  active  notice  shall  be  taken  of  it,  that  is  to  say,  whether  a 


4  NERVOUS    DISEASES 

voluntary  (and  not  merely  an  automatic)  movement  shall  or  shall 
not  take  place. 

Some  reflexes,  even  though  associated  with  conscious  sensory 
impressions  (for  example  the  vomiting  reflex,  or  the  sexual  reflex), 
cannot  be  inhibited.  This  is  possibly  owing  to  the  absence  of  anta- 
gonistic muscles  which  could  prevent  the  reflex.  But  other  reflexes 
can  be  inhibited  by  contracting  the  opposing  muscles  and  thereby 
fixing  the  part  which  would  otherwise  make  a  reflex  movement. 
Or  by  a  process  of  training,  a  stimulus  which  originally  induced 
one  particular  reflex  may  be  made  to  associate  itself  with  an 
entirely  different  response.     (See  "  Conditional  Reflexes.") 

Finally,  by  education,  a  motor  impulse  can  be  initiated  at  the 
cortical  motor  centre,  without  any  preceding  afferent  impulse 
from  the  part  to  be  moved.  All  movements  in  a  new-born 
infant  are  either  reflex  or  automatic,  and  only  gradually  does  the 
child  learn  to  call  in  antagonistic  muscles,  and,  by  an  effort  of 
the  will,  to  inhibit  reflex  acts  and  to  initiate  voluntary  ones. 

Certain  more  complicated  reflexes,  such  as  the  reflex  move- 
ments of  respiration,  have  their  centres  in  the  medulla ;  others, 
such  as  the  reflex  movements  of  the  heart  and  blood-vessels,  have 
their  lower  reflex  centres  in  the  sympathetic  ganglia,  but  can 
also  be  influenced  by  the  cerebro-spinal  nervous  system.  Others 
again,  such  as  the  movements  of  the  heart,  stomach,  and  intestine, 
can  be  performed  independently  of  the  central  nervous  system. 

Cranio-cerebral  Topography.— Figs.  3  and  4  are  diagrams  of 
the  cerebral  cortex,  on  its  convex  and  its  mesial  aspects.  It  is 
unnecessary  here  to  enumerate  in  detail  the  various  fissures  and 
sulci,  or  the  different  lobes  and  convolutions. 

It  is  important  to  be  able  to  identify,  on  the  surface  of  the 
cranium,  the  positions  of  the  Sylvian  and  Rolandic  fissures. 

The  Sylvian  fissure  corresponds  to  the  posterior  part  of  a  line 
drawn  from  the  fronto-malar  junction  to  the  lower  part  of  the 
parietal  eminence.  On  this  line  the  "  Sylvian  point,"  from 
which  the  ascending  and  antsrior  limbs  of  the  fissure  radiate,  is 
identified  by  drawing  a  line  from  the  fronto-malar  suture  hori- 
zontally backwards,  parallel  to  the  upper  border  of  the  zygomatic 
arch,  for  35  mm.,  and  from  ths  end  of  this  a  vertical  line  for 
12  mm.  upwards. 

The  central  or  Rolandic  fissure  starts  at  the  middle  line  above, 
from  a  point  1  cm.  (or  half  an  inch)  behind  the  mid-point  between 
the  nasion  (centre  of  naso-frontal  suture)  and  the  external  occipital 


ANATOMY    AND    PHYSIOLOGY  5 

protuberance  (or  inion).     It  runs  downwards  and  forwards,  along 
the  convex  surface  of  the  ?jrain,  in  the  direction  of  the  anterior 


f/if  i  frtrn/ii  sui  cu. 


PSn^LLEL    FI3SURJL 


fHKlETAL      -lULCUi 


Fig.  3. — Scheme  of  Cerebral  Localisation  (outer  surface). 

part  of  the  long  posterior  limb  of  the  Sylvian  fissure,  making  an 
angle  of  about  67 i  degrees,  i.e.  three-quarters  of  a  right  angle. 


C/tu.oso- ff/^KaiN/ti.  F/ssiyKS 


SUB-P/iKIET^U.   SULCUS 


COMMI3SUft^      ^NTEKICZ 


(»lJCAK.'Ha    F/SSUKC 


COi-L/iTEflAL     F/SSUK^. 


dY/ZUS    DE/^TATUS 
Oy/^S    HIPPOCAMPI 


Fig.  4. — Scheme  of  Cerebral  Localisation  (mesial  surface). 

with  the  middle  hne.  It  is  not  a  straight  line  but  forms  a  sinuous 
curve,  due  to  the  presence  of  two  buttresses  (mesial  and  lateral) 
on  its  anterior  wall,   producing   two   anterior   concavities.  ^    The 

^  Symington  and  Crymble,  J  cum.  of  Anat.  and  Physics,  vol.  xlvii.,   1913> 
p.  32L 


6  NERVOUS    DISEASES 

mesial  buttress  is  a  leg-trunk  buttress,  the  lateral  buttress  is  an 
arm  buttress  (see  Fig.  3). 

These  two  figures  also  show  diagrammatically  our  present 
views  on  cerebral  localisation.  It  should  be  particularly  observed 
that  the  motor  areas  in  the  pre-central  convolution  extend  back 
as  far  as  the  Rolandic  fissure  but  not  behind  it.  Not  only  by 
experimental  stimulation  in  anthropoid  apes/  and  in  certain  cases 
in  man,  but  also  by  histological  observation,^  it  has  been  shown 
that  the  posterior  or  sensory  wall  of  the  Rolandic  fissure  differs 


Fi^suTe^gf^sUuidLo 


FitJ.  5. — Diagram  of  cellular  structure  of  pre-  and  post-central  convolutions 

(after  Vogt). 


in  function  and  structure  from  the  anterior  or  motor  wall.  The 
anterior  wall  possesses  giant  pyramidal  cells,  and  has  no  granular 
layer,  whilst  the  posterior  wall  has  a  distinct  granular  layer,  with 
no  giant  cells  (see  Fig.  5). 

Another  point  to  remember  is  that  the  several  so-called  motor 
areas  are  not  sharply  marked  off  from  one  another  like  a  mosaic, 
but  overlap  ;  each  area  in  Figs.  3  and  4  signifying  that  stimulation 
of  that  point  produces  the  maximum  movement  of  the  particular 

^  Sherrington  and  Griinbamn,  Trans.  Path.  Soc.  Lond.,  1902,  vol.  liii. 
p.  127. 

-  Campbell,  A.  W.,  Histological  Studies  on  the  Localisation  of  Cerebral 
Function,  1905. 

Brodmarm,  K.,  Journ.  f.  Psychologie  und  Neurologic,  Bd.  ii.  p.  80. 


ANATOMY   AND   PHYSIOLOGY  7 

part  mentioned.  Moreover,  there  are  minor  variations  in  the 
extent  of  the  various  centres  in  different  individuals. 

The  chief  path  by  which  motor  impulses  are  conducted  from  the 
cortical  motor  areas  to  the  muscles  is  the  pyramidal  tract,  whose 
course  is  diagrammatically  indicated  in  Fig.  6.  From  the  motor 
cells  in  the  cortex  the  fibres  converge  through  the  corona  radiata 
into  the  great  strand  of  nerve-fibres  between  the  lenticular 
nucleus  externally  and  the  optic  thalamus  and  caudate  nucleus 
internally,  namely,  the  internal  capsule.  Fig.  7  shows  a  horizontal 
section  through  the  internal  capsule,  in  which  we  notice  that  it  has 
an  anterior  and  a  posterior  limb,  joining  each  other  at  an  obtuse 
angle,  the  genu  or  knee.  The  motor  fibres  for  the  leg  and  arm 
occupy  the  anterior  two-thirds  of  the  posterior  limb,  the  fibres  for 
the  tongue  and  mouth  are  at  the  genu,  those  for  the  face  just  in 
front.  But  the  order  in  which  these  different  strands  pass  through 
the  internal  capsule  is  not  quite  the  same  as  that  in  which  they 
started  from  the  cortex.  Thus  we  notice  that  immediately  behind 
the  fibres  for  the  lips  we  have,  from  before  backwards,  those  for  the 
shoulder,  elbow,  and  fingers  (not  fingers,  elbow,  shoulder),  then  for 
the  trunk,  and  lastly  for  the  hip,  knee,  and  toes.  We  also  notice, 
in  passing,  that  the  pathway  (thalamo-cortical)  of  the  sensory  fibres 
traverses  the  posterior  part  of  the  capsule,  and  that  behind  them 
again  are  the  visual  fibres.  The  sensory  fibres  probably  do  not 
form  a  separate,  compact  bundle,  but  are  partially  mingled  with 
some  of  the  motor  fibres  for  the  leg. 

Before  leaving  Figs.  6  and  7,  it  is  of  interest  to  study  briefly, 
with  their  help,  the  different  effects  produced  by  lesions  of  the 
pyramidal  motor  tract  at  various  levels. 

A  lesion  in  or  near  the  motor  cortex,  if  of  moderate  size,  will 
produce,  according  to  its  situation,  a  monoplegia  of  the  face,  arm, 
or  leg,  on  the  opposite  side  of  the  body.  A  somewhat  larger  lesion 
will  produce  a  brachio-facial  or  a  brachio-crural  monoplegia.  From 
the  proximity  to  the  middle  fine  of  the  cortical  centres  for  the  leg, 
a  mesial,  or  bilaterally  symmetrical,  lesion  may  imphcate  the  leg 
centres  of  both  sides,  producing  a  diplegia,  mainly  affecting  the 
legs.  (We  observe  that  facio-crural  monoplegia  without  implication 
of  the  arm  is  impossible  from  a  single  lesion.)  For  the  production 
of  a  complete  hemiplegia  of  face,  arm,  and  leg  a  cortical  lesion  must 
be  very  extensive.  But  in  the  internal  capsule  all  these  strands 
are  closely  crowded  together,  so  that  a  moderate-sized  capsular 


NERVOUS    DISEASES 


CRUS  CEREBRI 
Level  of  .T"^ Nerve 


pojsrs 

Leveb  oT Fou:iaLIIerve 


■--  FojcixiL  Nerve 


Face 


CrossecLFyramidaLlhoLCt 


MEDULLA 
Mypog  lossaL  Nerve 

-DirectFyrcunioiaL  Tract 
SPINAL  CORD 


Leg- 


Fl&.  6. — Diagram  of  Pyramidal  Tract  and  its  course  through  the  brain 

and  cord. 


ANATOMY    AND    PHYSIOLOGY  9 

lesion  can  produce  a  complete  hemiplegia,  whereas  a  capsular 
lesion  small  enough  to  cause  a  mere  monoplegia  is  well-nigh 
impossible. 

If   the  capsular  lesion  be  in  the  region  of  the  genu  we  have 
hemiplegia  of  face,  arm,  and  leg.     And  moreover,  from  paralysis 


CojidaJbe,  NvLcle.  as 

■jAejiUcuZarJtrucleus 
CloaistrizjTz/ 

Sensory  TLbres 
SylvLouvJ'issura 


VvsumL  Fiires  of 
Optbc  RauiiaUon,. 


Fctrieto-  OccipitaLFissura 


Fig.  7.^Horizontal  section  through  right  cerebral  hemisphere,  showing 
position  of  the  various  strands  in  the  internal  capsule.  (After  Beevor 
and  Horsley.) 

of  the  muscles  which  rotate  the  head  and  eyes  to  the  opposite  side, 
the  patient  has  "  conjugate  deviation "  of  the  head  and  eyes 
towards  the  side  of  the  lesion,  owing  to  unopposed  action  of  the 
muscles  suppHed  by  the  intact  hemisphere. 

If,  on  the  other  hand,  the  capsular  lesion  be  farther  back  along 
the  posterior  limb  of  the  capsule,  the  hemiplegia  will  affect  the  leg 


10 


NERVOUS    DISEASES 


much  more  than  the  arm,  and  the  face  only  slightly  ;  whilst,  owing 
to  interference  with  the  sensory  tract,  which  hes  between  the 
motor  and  the  visual  fibres,  there  will  now  be  hemiansesthesia 
also. 

Lastly,  if  the  lesion  be  at  the  extreme  posterior  end  of 
the  capsule,  there  will  be  not  only  hemiansesthesia  but  also 
hemianopia  from  interruption  of  the  visual  fibres.  Here  again 
we  note  that  it  is  impossible  for  a  single  capsular  lesion  to  produce 
at  the  same  time  hemiplegia  and  hemianopia  without  also  pro- 
ducing hemiansesthesia.     If   a   patient   with   hemianopia   is   also 


Figs.  8  and  8a. — Case  of  tumour  at  posterior  pole  of  right  occipital  lobe,  in 
which  decompressive  trephining  had  been  performed.  A  large  hernia  cerebri 
developed,  and  subsequently  a  hsemorrhage  occurred  anterior  to  the  tumour, 
within  the  substance  of  the  hernia. 

hemiplegic  but  without  hemiansesthesia,  we  should  diagnose  two 
separate  lesions. 


Figs.  8  and  8a  are  from  such  a  case,  in  which  a  patient  with  left 
hemianopia  due  to  a  tumour  of  the  right  occipital  lobe  subsequently 
became  totally  hemiplegic  with  only  a  faint  trace  of  hemiansesthesia. 
The  diagnosis  of  two  distinct  lesions  was  confirmed  at  the  autopsy  : 
the  original  tumour  in  the  posterior  end  of  the  occipital  region  being 
separated  by  an  intervening  healthy  zone  from  a  large  hsemorrhage 
farther  forward -in  the  hemisphere. 

A  lesion  of  the  crus  cerebri  will  tend  to  implicate  the  third  cranial 
nerve  on  the  side  of  the  lesion,  producing  at  the  same  time  a  hemi- 
plegia of  face,  arm,  and  leg  on  the  opposite  side.  This  so-called 
"  Weber's  S5nidrome  "  is  one  variety  of  "  crossed  paralysis." 


ANATOMY    AND    PHYSIOLOGY  11 

A  unilateral  lesion  of  the  pons  at  the  level  of  exit  of  the  facial 
nerve  will  produce  another  "  crossed  paralysis,"  viz.  : — facial  palsy 
on  the  side  of  the  lesion  with  hemiplegia  of  the  arm  and  leg  of  the 
opposite  side.  And  if  at  the  same  time  the  nucleus  of  the  sixth 
cranial  nerve  be  implicated  (which  is  not  unusual,  since  the  facial 
nerve  hooks  round  the  sixth  nucleus  within  the  pons),  we  have 
nuclear  palsy  of  the  sixth  nerve,  facial  palsy  on  the  same  side, 
and  hemiplegia  of  the  arm  and  leg  on  the  opposite  side  : — the 
"  Millard-Gubler  syndrome." 

Unilateral  lesions  of  the  pons  or  medulla  below  the  level  of  the 
facial  nerve  leave  the  face  unaffected  and  produce  only  a  hemiplegia 
of  arm  and  leg.  And  a  unilateral  lesion  of  the  spinal  cord  below  the 
cervical  enlargement  will  produce  a  monoplegia  of  the  leg  on  the 
side  of  the  lesion  without  affection  of  the  arm.  It  will  also  produce 
some  anaesthesia  of  the  opposite  leg.  Such  motor  paralysis  of  one 
leg  and  sensory  paralysis  of  the  other  is  called  "  Brown-Sequard 
paralysis,"  to  which  we  shall  return  later. 

Fig.  9  is  a  diagram  representing  the  tracts  in  the  spinal  cord 
of  chief  clinical  interest.  There  are  also  other  ascending  and 
descending  tracts  of  minor  importance,  which  we  have  omitted 
from  the  diagram  for  the  sake  of  simplicity. 

The  pyramidal  tracts  are  by  far  the  most  important  descending 
tracts  in  the  cord,  for  they  convey  voluntary  motor  impulses  down- 
wards from  the  motor  cortex  towards  the  anterior  cornua.  The 
pyramidal  fibre  does  not  actually  join  the  anterior  cornu,  but  ends  in 
the  region  of  the  posterior  cornu,  whence  a  short  intermediate  con- 
necting-cell and  fibre  run  forward,  linking  it  to  the  anterior  cornual 
cell  (see  Fig.  2).  Most  of  the  voluntary  motor  impulses  decussate 
at  the  lower  end  of  the  medulla  and  traverse  the  crossed  pyramidal 
tract  in  the  lateral  column  ;  a  few  run  in  the  direct  pyramidal  tract 
and  cross  over  later  within  the  cord  itself.  A  few  pyramidal  fibres 
also  run  down  in  the  ipso-lateral  pyramidal  tract  (which  we  might, 
somewhat  paradoxically,  call  the  uncrossed  crossed-pyramidal  tract). 
These  fibres  probably  do  not  cross  over,  but  supply  motor  impulses 
to  the  ipso-lateral  leg.  They  account  for  the  occurrence  in  hemi- 
plegia of  certain  phenomena  on  the  opposite,  "  non-paralysed " 
side,  such  as  paresis,  increased  deep  reflexes,  and  sometimes  con- 
tractures in  the  "  healthy  "  lower  hmb. 

In  addition  to  the  great  pyramidal  or  cortico-spinal  tracts,  there 
are  other  minor  tracts  which  enter  the  spinal  cord  from  above. 


12 


NERVOUS    DISEASES 


These  are  derived  from  sub-cortical  motor  centres,  and  constitute 
subsidiary  subcortico- spinal  tracts.  They  end  among  the  cells  of 
the  anterior  horns,  and  provide  a  mechanism  for  the  performance 
of  certain  automatic  acts  which  may  still  be  possible  when  voluntary 
motor  power  is  lost,  as  in  pyramidal  disease.  These  subcortico- 
spinal  tracts  also  serve  to  maintain  a  normal  degree  of  tonus  in 


Fig.  9. — Diagram  of  Tracts  in  the  Spinal  Cord. 


1.  Crossed    pyramidal  tract  (descending) 

and  Spino-thalaraic  tract  (ascending). 

2.  Direct  pyramidal  tract. 

3.  Postero-internal  tract  (GoU). 

4.  Postero-external  tract  (Burdach). 


5.  Direct  or  dorsal  cerebellar  tract. 

6.  Ventral  cerebellar  tract  (Gowers). 

7.  Lissauer's  marginal  zone. 

8.  Lateral  ground-bundle. 

9.  Anterior  ground-bundle. 


the  voluntary  muscles,  thus  constituting  an  apparatus  which 
(largely  influenced  by  afferent  stimuli,  especially  from  the  semi- 
circular canals)  facilitates  equilibration  during  such  acts  as  stand- 
ing or  walking.  Of  these  tracts  the  most  important  are  the  follow- 
ing (see  Fig.  10)  : — 

1.  The  rubrospinal  or  pre-pyramidal  tract  (Monakow's  bundle). 
— This  tract  arises  in  the  red  nucleus  of  the  crus  cerebri,  decussates 
almost  at  once  in  the  tegmentum,  and  descends  in  the  contra-lateral 


ANATOMY    AND    PHYSIOLOGY 


13 


N.Caiulai 


A  — Crossed  pyramidal. tract. 
B  =  Direct  pyramidal  tract. 
l=Rubro-spinal  tract  ( —  -) 
2=Tecto-spinal  tract   ( — — ) 
3  =  Vestibulo-spiual  tract  (....) 

t.l  p=Fasciculus  longitudinalis 
posterior. 

f.l.v  =  Fasciculus  longitudinalis. 
ventralis. 

Iera  =  Fillet  or  lemniscus. 


3|. 

lem 


CRUS  CERKBR] 


PONS 


MEDULLA 


SPINAL  CORD 


Fig.  10. — Cortico-spinal  and  sub-cortico-spinal  tracts. 


14  NERVOUS    DISEASES 

side  of  the  pons  and  medulla  to  the  lateral  column  of  the  spinal  cord, 
where  it  lies  ventral  to  the  crossed  pyramidal  tract. 

2.  The  tedo-sfinal  tract  or  ventral  longitudinal  bundle. — This 
arises  in  the  mid-brain  from  the  anterior  corpus  quadrigeminum, 
crosses  over  in  Meynert's  "  fountain  "  decussation  beneath  the 
Sylvian  aqueduct,  and  then  runs  down  the  contra-lateral  side  of 
the  formatio  reticularis  to  the  ventral  column  of  the  spinal  cord. 

3.  The  vestibulospinal  tract  or  dorsal  longitudinal  bundle. — This 
arises  from  the  accessory  vestibular  nucleus  of  Deiters  within  the 
pons,  and  passing  downwards  mainly  on  the  ipso-lateral  side  of  the 
spinal  cord  in  the  ventral  column ,  ends  amongst  the  anterior  cornual 
cells. 

In  the  adult  the  ventral  and  dorsal  longitudinal  bundles  are 
indistinguishable  from  each  other  on  section  of  the  medulla  or 
spinal  cord,  but  they  myelinate  at  different  periods  of  development, 
and  can  thus  readily  be  differentiated  in  the  foetus. 

4.  The  fonto-spinal  tract. — This  is  derived  from  cells  of  the 
formatio  reticularis  of  the  pons.  Part  of  it  runs  down  the  ventral 
column  of  the  ipso-lateral  side,  whilst  part  decussates  in  the  raphe  of 
the  medulla  and  enters  the  opposite  lateral  column  of  the  spinal  cord. 

Certain  of  the  extra-pyramidal  tracts,  probably  the  vestibulo- 
spinal and  ponto-spinal,  have  a  special  action  in  maintaining  a 
condition  of  tonus  in  the  extensor  muscles,  especially  of  the  lower 
limbs.  1  Therefore  in  a  pure  pyramidal  lesion,  as  in  ordinary  hemi- 
plegia, these  extra-pyramidal  tracts,  being  now  unopposed,  pro- 
duce tonic  rigidity  of  the  extensor  muscles  with  a  characteristic 
posture  of  the  lower  limbs. 

Sensory  Paths. — According  to  Head,  Rivers,  and  Sherren,^ 
the  various  afferent  impulses  from  the  periphery,  on  their  way 
towards  the  spinal  cord,  do  not  run  indiscriminately  along  the 
afferent  nerves  but  are  conducted  along  several  distinct  classes  of 
nerve  fibres.  According  to  these  observers,  common  sensation  is 
a  complex  affair,  based  on  three  kinds  of  sensibility  : — 

1.  Deep  sensibility,  a  variety  which  takes  cognisance  of  deep 
pressure,  and  which,  if  that  pressure  be  excessive,  is  capable 
of  producing  a  sensation  of  pain — •"  pressure -pain."  Deep  sensi- 
bility also  includes  sensations  from  muscles  and  tendons,  from 
joints,   and  the  vibration-sense   (see   later,   p.   203).     The   fibres 

1  Walshe,  Brain,  1914,  vol.  xxxvii.  pp.  269-334. 

2  Brain,  1905,  pp.  99-115. 


ANATOMY    AND    PHYSIOLOGY 


15 


conducting  deep  sensibility  run  along  with  the  nerves  of  the  muscles 
and  tendons.  So  long  as  these  fibres  are  intact,  even  though  the 
skin  be  totally  analgesic,  the  patient  is  able  to  appreciate  the 
pressure-touch  and  pressure-pain  of  a  blunt  pencil,  the  vibration 
of  a  tuning-fork,  and  the  position  of  his  joints  on  passive  movement. 


FyramjidalTract/ 


Sense  oFActiye  Muscular  CantrojcUjOTV. 
Joint  Sense. 

-TenxpercUure  caidb  Fodru. 

■Tactile  iSense. 


Fig.  11. — Diagram  illustrating  the  course  of  the  various  sensory  paths  in 
the  spinal  cord. 


The  fibres  for  deep  sensibihty  are  not  destroyed  by  division  of  all 
the  sensory  nerves  to  the  skin. 

2.  Protofathic  cutaneous  sensibility,  a  variety  which  responds 
to  painful  cutaneous  stimuli  (pricking,  faradic  stimulation),  also  to 
extremes  of  cold  and  heat,  like  freezing  and  burning  (temperatures 
of  45°  C.  and  over,  and  of  10°  C.  and  under).  These  protopathic 
fibres  from  the  skin  are  the  first  to  regenerate  after  injury  to  a 


16  NEKVOUS    DISEASES 

cutaneous  nerve,  so  that  tlie  protopathic  sensations  are  the  earliest 
to  recover  as  a  cutaneous  nerve  heals. 

3.  Epicritic  cutaneous  sensibility,  whose  fibres  are  the  slowest 
to  recover  after  injury.  This  group  includes  the  appreciation  of 
light  touches,  of  cutaneous  locahsation  (the  discrimination  of  two 
points  of  an  opened  compass  as  being  separate),  the  recognition  of 
finer  differences  of  temperature — not  merely  between  hot  and 
cold,  but  between  warm  and  cool.  Epicritic  sensibihty  is  normally 
absent  at  the  glans  penis. 

These  differences,  it  should  be  noted,  apply  only  to  the  extra- 
spinal  portion  of  the  sensory  paths,  i.e.  to  the  peripheral  nerves. 

All  the  sensory  impulses,  whether  conveying  sensations  of 
touch,  temperature,  or  pain  from  the  skin,  sensation  of  active 
muscular  contraction  from  the  muscles  (kingesthetic  sense),  or 
sensations  from  the  joints  or  bones;  enter  the  spinal  cord  through 
the  posterior  roots,  as  indicated  in  Fig.  11. 

Once  the  afferent  impulses  enter  the  spinal  cord,  it  is  no  longer 
a  question  of  deep,  epicritic,  or  protopathic  sensation  ;  they  now 
become  redistributed  in  simpler  fashion.  Thus  all  sensations  of 
temperature  run  together  in  one  tract,  whether  they  reached  the 
cord  by  the  protopathic  or  the  epicritic  route  :  similarly  all  sen- 
sations of  pain  run  together  in  the  cord,  whether  they  were 
protopathic,  or  "  deep  "  in  the  peripheral  nerves,  and  so  on.  This  is 
indicated  in  the  following  scheme  : — 

Paths  in  Spinal  Cord.  Paths  in  Peripheral  Nerves. 

Deep     .    .      a  Pressure. 


/? 


Posterior  Column \,p..,  J^  / (3  Light  Touches. 

Lateral  Column     J  ^-'1'-"''=  ly  U  Localisation. 


Epicritic   .  -,  S  Differences  in  Size. 

,rp„    „  ,,  f,„,„/e  vf  Moderate  dilferences  of  Temperature, 

lempeiatuie  ^^  ^  ,^  Extreme  differences  of  Temperature. 

'  Pi-ntrvTin+Viin  J  _  _ 


Lateral  Column    -•.  ,       Protopathic 

[pai„  J  I        electricity). 


,       r.ui,opd,i,iuus      Cutaneous  Pain  (pricks,  freezing,  burns. 


/  Muscles 
Posterior  Column-,  Joints 


Deep 


6  Pressure-Pain. 

I  Lengthening  or  Shortening  of  Muscles. 

K  .Joints — passive  movements. 


i^Bont)!"  ^  U  Vibration  (tuning-fork), 

Of  these  various  impulses,  the  fibres  conveying  sensations 
from  the  muscles  and  joints,  together  with  the  smaller  part  of  the 
fibres  for  tactile  sensation,  ascend  in  the  posterior  column  to  the 
gracile  and  cuneate  nuclei  of  the  same  side  of  the  medulla.  Most 
of  the  fibres  for  tactile  sense,  together  with  those  for  temperature 


ANATOMY    AND    PHYSIOLOGY  17 

and  pain,  cross  in  the  anterior  commissure  to  the  opposite  side 
(these  crossed  fibres  not  coming  directly  from  the  posterior  root, 
but  through  the  relay  of  another  cell  in  the  posterior  horn)  and 
ascend  the  cord  in  the  opposite  lateral  column,  in  the  spino- 
thalamic tract.  Thus  the  lateral  column  conducts  not  only 
pyramidal  motor  impulses  coming  down,  but  also  spino-thalamic 
ascending  impulses  of  touch,  temperature,  and  pain. 

The  upward  course  of  the  various  sensory  fibres  through  the 
medulla  and  pons  is  somewhat  compUcated,  and  not  yet  entirely 
settled,  but  the  most  probable  arrangement  is  shown  in  Fig.  12. 

Most  of  the  fibres  for  touch  cross  the  middle  line  in  the  spinal 
cord,  as  already  explained,  and  then  pass  directly  upwards  in  the 
spino-thalamic  tract  of  the  lateral  column  and  into  that  part  of  the 
medulla  called  the  formatio  reticularis.  The  formatio  reticularis 
leads  the  fibres  up  through  the  pons  and  cms  to  the  ventro-lateral 
region  of  the  optic  thalamus,  and  thence  they  pass  through  the 
posterior  limb  of  the  internal  capsule  to  the  sensory  cortex  behind 
the  fissure  of  Rolando. 

As  the  sensory  tract  traverses  the  pons  it  passes  along  the 
inner  side  of  the  sensory  spinal  root  of  the  trigeminal  nerve  of  the 
same  side.  Thus  a  unilateral  lesion  of  the  formatio  reticularis 
just  below  the  exit  of  the  fifth  or  trigeminal  nerve  will  produce  a 
"  crossed  anaesthesia,"  i.e.  ansesthesia  of  the  face  on  the  side  of 
the  lesion,  and  of  the  arm,  leg,  and  trunk  of  the  opposite  side.  But 
higher  up  the  pons  the  sensory  fibres  from  the  face  also  cross  the 
middle  line,  so  that  a  lesion  of  the  formatio  reticularis  in  the  crus 
cerebri  will  now  cause  complete  hemianaesthesia  of  face,  arm,  and 
leg  (see  Fig.  13). 

The  fibres  for  temperature  and  pain,  entering  by  the 
posterior  root,  pass  into  the  grey  matter  of  the  posterior  cornu. 
There  they  start  afresh  and  cross  to  the  opposite  side  of  the 
cord,  ascending  in  the  opposite  lateral  colunm  near  the  crossed 
tactile  fibres.  On  reaching  the  medulla,  they  diverge  from  the 
tactile  fibres  and  pass  to  the  outer  side  of  the  olivary  body,  close 
to  the  lateral  margin  of  the  medulla  and  intermingled  with  the 
fibres  of  Gowers'  tract.  They  then  leave  the  region  of  Gowers' 
tract  and  pass  upwards  through  the  pons,  gradually  inclining  to- 
wards the  other  sensory  tracts  and  ultimately  ascending  with  them 
to  the  ventro-lateral  part  of  the  optic  thalamus  and  thence  through 
the  internal  capsule  to  the  cortex.     Gowers'  tract  (the  ventral 

B 


18 


NERVOUS    DISEASES 


CouuuiaJteNvuclews 


Optic  Thalamuus 


FvrmatijjlletLcujLans  ----. 
Fillet 
Kexi  NiLcleiLs   ' " 


CorpubsRestiforme. 

Fillet - 
V'jferve.---^ 

Fibres  ofSpinalRoot  of  V 


Corpus  Pestiforme-  - 
TornuxtwRetLciLljiris  - 

SpuhoLRootofV 
Tart  aTGowersTraLCt^—. 
Fillet- -i 


PONS 

Level  of  V Nerve. 


Jfucleiis  Gracilis  - 
NvLcleus  CunealMS 

SpizuiLRoot  of  V 

Direct  CerebeVLarTrouct 

Part  of  Gowers' Tract 

Fillet  - 


ToLctile  Sense  {Uncrossed/) 
Joint  Sense  do. 

Kinaesthetic  Sense         do 

PosterLorRoot j 


i  --lenbiculxjrNvudUus 


PONS 
level  of  8^ Nerve. 


EcpiibJbrLLLnv 
(Direct  Ceretellar  Troucb) 


MEDULLA 

Formalio  ReticuZaris. 


Tactile  Sense  (Crossedj 
Temperalure  &Pairv  (Cross ed>) 

:^jj. En uiUbriunv   (Uhcrossedj 

T'V         SPINAL  CORD 


Fig.  12. — Diagram  of  Chief  Sensory  Tracts  in  Spinal  Cord,  Medulla, 
Pons,  and  Cerebrum. 


ANATOMY    AND    PHYSIOLOGY 


10 


cerebellar),  now  separate  from  the  temperature  and  pain  fibres  in 
the  upper  part  of  the  pons,  hooks  sharply  backwards  and  enters 
the  cerebellum  from  above,  through  the  superior  peduncle. 

The  sensory  fibres  from  muscles  and  from  bones,  together  with 
the  uncrossed  minority  of  tactile  fibres,  ascend  uncrossed  in  the 


VJTerye 


Atttv. 


.  Leff. 
Fl&.  13. — Course  of  Sensory  Fibres  in  the  Pons  (Starr). 

A.  Lesion  causing  right  hemianfesthesia. 

B.  Lesion  causing  "  alternate  hemianiesthesia  "  of  left  face  and  right  side  of  body. 


posterior  column  of  the  cord  to  the  nucleus  gracihs  and  nucleus 
cuneatus,  the  nucleus  gracilis  receiving  the  fibres  from  the  lower 
limb,  the  nucleus  cuneatus  those  from  the  upper  hmb.  Some 
impulses  pass  via  the  restiform  body  to  the  cerebellum  and  thus, 
although  not  destined  to  give  rise  to  conscious  sensations,  they 
influence  co-ordination  and  muscular  tonus.     The  remainder  of  the 


20  NERVOUS    DISEASES 

sensory  fibres  in  the  posterior  columns,  after  reaching  the  nucleus 
gracilis  and  nucleus  cuneatus,  pass  upwards,  and  cross  the  middle 
line  in  the  internal  arcuate  fibres,  forming  the  superior  sensory 
decussation  of  the  fillet  (contrast  this  with  the  spinal  decussation 
of  the  thermal,  pain,  and  the  majority  of  the  tactile  fibres).  The 
sensory  fibres  from  the  leg,  passing  through  the  nucleus  gracilis, 
cross  lower  down  than  those  from  the  arm,  which  go  through  the 
nucleus  cuneatus.  Having  crossed  to  the  opposite  side  and  reached 
the  fillet,  a  flattened  strand  of  fibres,  they  pass  upwards  in  that 
tract  not  far  from  the  thermal  and  pain  fibres.  The  main  mass 
of  the  tactile  fibres  ascends  through  the  crus  cerebri  to  the  optic 
thalamus,  and  thence  through  the  internal  capsule  to  the  sensory 
cortex,  which  lies  behind  the  Rolandic  fissure,  ^  the  sensory  centres 
for  the  face,  arm,  leg,  &c.,  being  situated  opposite  the  corre- 
sponding motor  centres,  on  the  other  side  of  the  fissure. 

All  sensory  impulses  which  reach  the  thalamus  are  there  grouped 
afresh  and  redistributed  in  two  directions.  Some  impulses  ascend 
to  the  cortex  cerebri ;  others  terminate  in  the  grey  matter  of  the 
thalamus  itself,  which  thus  forms  an  important  sub-cortical  sensory 
centre,  subserving  certain  fundamental  elements  of  sensation, 
especially  the  feehng-tones  of  'pleasure  and  pain  and  of  certain 
visceral  sensations.  The  cortex,  on  the  other  hand,  is  the  organ 
for  focussing  attention  upon  sensory  stimuH  and  for  discriminating 
between  their  finer  varieties.  The  cortex  also  stores  up  memories 
of  past  impressions. 

We  have  stiU  to  consider  another  tract,  which  conducts  sensory 
fibres  for  the  sense  of  equilibrium.  This  tract  does  not  commence  in 
the  posterior  root-ganglion  but  arises  as  an  "  endogenous  "  tract 
within  the  cord.  Arising  from  the  cells  of  Clarke's  column  at  the 
base  of  the  posterior  horn,  it  constitutes  the  direct  (or  dorsal) 
cerebellar  tract  and  ascends,  uncrossed,  into  the  restiform  body 
and  cerebellum,  terminating  among  the  Purkinje  cells  of  the 
cerebellar  cortex. 

Before  leaving  the  motor  and  sensory  tracts  within  the  central 
nervous  system  it  will  be  useful  to  mention  the  symptoms  produced 
by  a  lesion  of  one  lateral  half  of  the  spinal  cord.     Such  a  lesion 

1  Faradic  stimulation  of  the  post-Rolandic  cortex  in  the  human  subject* 
produces  sensory  phenomena  which  are  referred  to  the  hmb,  or  other  part  of 
the  body,  corresponding  to  the  particular  cortical  centre. 

*  Van  Valkenburg,  Zeitschrift  fur\die  ges.  Neurologie  imd  Psychiatrie,  xxiv.  Heft  2^and  3. 


ANATOMY    AND    PHYSIOLOGY 


21 


is  most  commonly  the  result  of  a  stab  in  the  back  ;  less  commonly  it 
is  produced  by  bullet-wounds,  fractured  spine,  caries,  or  by  chronic 
diseases  of  the  spina]  cord  itself.     The  syndrome  which  results  is 


^CNSAT/OmJ/VT  L£¥'£l 


Fig.  14. — Diagram  illustrating  the  symptoms  resulting  from  a  left-sided 
hemi-section  of  the  spinal  cord  (Brown-Sequard  syndrome). 


known  as  Brown-S^quard  paralysis,  and  it  will  be  readily  understood 

by  reference  to  Figs.  11  and  14.     The  symptoms  are  as  follows  : — 

(1)  On  the  side  of  the  lesion  we  have,  from  interruption  of  the 


22  NERVOUS    DISEASES 

motor  tract,  motor  paralysis  of  the  corresponding  leg,  with  an 
extensor  plantar  reflex  from  the  outset  and,  later  on,  exaggeration 
of  the  deep  reflexes.  There  is  a  slight  and  transient  elevation  of 
temperature,  owing  to  the  interruption  of  vaso-motor  fibres  which 
descend  in  the  lateral  column.  There  is  loss  of  sense  of  position 
on  passive  movement  of  the  limb,  loss  of  power  of  estimating 
weights,  and  loss  of  "  vibration  sense  "  (tested  by  a  tuning-fork) 
in  the  bones  of  the  paralysed  leg,  due  to  interruption  of  the  un- 
crossed fibres  from  the  posterior  roots  below  the  lesion,  which 


CULMEN 


F/SSU/ZE. 


Fig.  15. — Vertical  mesial  section  through  cerebellum.     Pons  and  Medulla. 


ascend  in  the  posterior  column.  The  skin  of  the  paralysed  leg  is 
not  anaesthetic,  but,  just  at  the  level  of  the  lesion,  there  is  around 
the  trunk  a  narrow  zone  of  total  anaesthesia  (to  touch,  temperature, 
and  pain)  from  lesion  of  the  fibres  of  the  posterior  root  or  roots 
at  the  level  of  the  injury.  Finally,  in  cases  with  an  abrupt  onset, 
there  is  a  narrow  zone  of  hypereesthesia  above  the  ansesthetic  zone, 
perhaps  due  to  local  irritation  of  the  lowest  unsevered  posterior- 
root  fibres  in  the  cord,  close  above  the  lesion  ;  but  this  explanation 
is  in  dispute. 

(2)  On  the  side  opposite  to  the  lesion  there  is  no  motor  paralysis. 


ANATOMY    AND    PHYSIOLOGY 


23 


But  there  is  loss  of  cutaneous  sensation  to  temperature  and  pain 
(completely),  and  to  touch  (partially),  in  the  non-paralysed  lower 
limb  and  in  the  corresponding  half  of  the  trunk  up  to  the  level  of 
the  lesion.  There  is  a  zone  of  hypersesthesia  above  the  anajs- 
thetic  area,  as  on  the  side  of  the  injury.  Motor  power  is  unim- 
paired, so  also  is  the  sensation  of  position  on  active  or  passive 
movement  of  the  limb. 

Cerebellum. — 

The  cerebellum  consists  of  two  lateral  lobes  or  hemispheres  joined 
together  by  a  median  lobe  or  vermis.     Between  the  two  hemispheres, 


LOBUtUS  ca/^TR^i/s 


PfilM/iR.Y   OK. 


CUl^US 


CUIMEH 
Fig.  16. — Cerebellum  :  upper  surface. 

on  the  ventral  aspect,  is  a  deep  median  fossa  or  vallecula,  whose  floor 
is  formed  by  the  projection  of  the  inferior  vermis.  In  the  posterior 
part  of  this  fossa  lies  the  medulla,  in  front  of  which  are  the  pons  and 
crura  cerebri  running  forward  through  the  anterior  cerebellar  notch. 
The  upper  surface  of  the  middle  lobe  (superior  vermis)  passes  into  the 
lateral  lobe  without  any  distinct  line  of  demarcation,  whereas  its  under 
surface  (inferior  vermis)  forms  a  mesial  projection  in  the  vallecula, 
sharply  marked  off  from  the  hemispheres  by  deep  antero-posterior 
grooves,  one  on  each  side.  The  cortex  of  vermis  and  lateral  lobes  is 
deeply  folded  into  fine  leaves  or  lamina?,  separated  by  closely-set 
fissures  running  sinuously,  more  or  less  parallel  with  each  other,  some 
of  them  running  obliquely  between  the  others. 


24 


NERVOUS    DISEASES 


The  vermis,  at  an  early  stage  of  development,  is  divided  by  the 
primary  (or  preclival)  fissure  into  an  anterior  and  a  posterior  lohe.  In 
the  adult  condition  it  is  still  further  subdivided  into  finely  laminated 
lobules,  which  are  best  seen  on  sagittal  section  (see  Fig.  15).  In 
front  of  the  primary  fissure  we  have  three  lobules  :  lingula,  lohulus 
centralis,  and  culmen,  from  before  backwards. .  Behind  the  primary 
fissure,  in  the  posterior  lobe,  matters  are  much  more  complex,  and 
there  are  six  lobules :  clivus,  folium  vermis,  tuher  vermis,  pyramis, 
uvula,  and  nodulus.  These  form,  as  it  were,  branches  of  a  tree  {arhcr 
vitce)  whose  trunk  is  planted  on  the  roof  of  the  fourth  ventricle,  with  its 
most  anterior  branch,  the  lingula,  on  the  anterior  medullary  velum,  in 
front,  and  its  most  posterior  branch,  the  nodulus,  on  the  posterior 
medullary  velum  behind. 

The  cerebellar  hemispheres,  like  the  vermis,  are  divided  by  the 
primary  fissure  into  anterior  and  posterior  lobes,  and  for  each  lobule 


Fig.  17. — Cerebellum  :  posterior  surface. 

of  the  vermis  there  is  a  corresponding  lobule  of  the  hemisphere  with 
which  it  is  continuous.  Thus  in  the  anterior  lohe,  on  each  side  from 
before  backwards,  there  is  ^h^frcenulum  linguae,  the  ala  lohuli  centralis, 
and  the  lohulus  lunatus  anterior,  seen  on  the  upper  and  anterior  sur- 
faces (Figs.  16  and  17),  whilst  the  more  complex  posterior  lohe  has  the 
lohulus  lunatus  posterior,  the  lohulus  semilunaris  superior,  followed,  on 
the  posterior  and  postero-inferior  aspects,  by  the  lohulus  semilunaris 
inferior,  lohulus  gracilis,  lohulus  hiventer,  and  the  tonsil  (Fig.  18). 
Laterally  situated  from  the  lobulus  biventer  and  tonsil,  and  lying 
in  a  deep  sulcus  immediately  behind  the  middle  peduncle  on  each  side, 
is  a  small  irregular  lobule,  the  flocculus.  The  various  fissures  of  the 
cerebellum  are  indicated  on  Figs.  15  to  18. 

Within  the  white  matter,  at  a  distance  from  the  cortex  and  analogous 
in  some  respects  to  the  basal  ganglia  of  the  cerebrum,  there  are  several 
important  masses  of  grey  matter  from  which  various  efferent  tracts 
lead  to  other  parts  of  the  brain.     Of  these  the  chief  are  the  corpora 


ANATOMY    AND    PHYSIOLOGY 


25 


dentata,  two  hollow  cruuipled  sacs,  one  within  each  lateral  lobe  ;  the 
roof  nuclei  within  the  middle  lobe ;  the  nuclei  glohosi  and  the  nuclei 
emholiformes,  bilaterally  situated,  between  the  roof  nucleus  and  the 
dentate  nucleus  (see  Fig.  19) ;  and  the  nuclei  of  JJeiters,  or  accessory 
vestibular  nuclei,  within  the  pons,  one  on  each  lateral  aspect.  Deiters' 
nucleus  has  several  highly  important  connections,  some  afferent,  from 
the  vestibular  nerves  and  the  cerebellar  cortex  ;  others  from  the  ocular 
nuclei  (third  and  sixth)  vid  the  dorsal  longitudinal  bundles  ;  others, 
again,  efferent,  to  the  anterior  cornual  cells  of  the  same  side  of  the 
cord,  through  the  vestibulo-spinal  tract. 

Each  lateral  lobe  has  three  peduncles — superior,  middle,  and 
inferior  (Fig.  20) — consisting  of  fibres  some  of  which  run  towards 
the  cerebellum  (cerebello-petal),  others  away  from  it  (cerebello-fugal). 


lOBULI 
CENTRALIS 


LOBULU5    CENTKALI5 


LIHGULA 

SUP   PE.DUNCLB 


>R£-CL/Ml)  fissure 


HOR/ZOHT/^llS 


FLOCCUlUS 


Ui^UL/) 

Fig.  18. — Cerebellum  :  Antero-iuferior  or  ventral  surface. 


The  cerebello-petal  fibres  terminate  around  the  large  Purkinje 
cells  of  the  cerebellar  cortex,  which  is  essentially  a  receiving  platform. 

In  the  inferior  peduncle,  or  restiform  body,  which  connects  the 
cerebellum  with  the  medulla  and  spinal  cord,  all  the  paths  are  cerebello- 
petal,  leading  to  the  cerebellar  cortex.  Amongst  them  the  most  im- 
portant is  the  dorsal  or  direct  cerebellar  tract,  conveying  impulses  of 
equilibrium  from  the  ipso-lateral  side  of  the  spinal  cord,  and  the 
arcuate  fibres,  from  the  posterior  column  nuclei  of  both  sides,  and  from 
the  inferior  olive  of  the  contra-lateral  side.     (See  Fig.  20.) 

Another  important  cerebello-petal  path  from  the  spinal  cord  is  the 
ventral  cerebellar  tract  of  Gowers,  which  has  a  long  course  within  the 
medulla  and  pons,  traversing  them  from  below  upwards  and  ultimately 
hooking  downwards  again,  to  enter  the  cerebellum  from  above,  through 
the  superior  peduncle. 


26 


NEEVOUS   DISEASES 


Cerebello-petal  fibres  from  the  frontal,  parietal,  and,  above  all, 
the  temporal  lobe  of  the  cerebrum,  run  downwards  through  the  superior 
peduncle  to  the  pontine  nuclei  (formatio  reticularis)  on  the  ipso-lateral 
side.  From  the  cells  of  the  pontine  formatio  reticularis  new  cerebello- 
petal  fibres  start  again,  constituting  the  middle  peduncle,  or  transverse 
fibres  of  the  pons,  crossing  the  middle  line  and  ending  in  the  contra- 
lateral cerebellar  cortex.  Other  cerebello-petal  fibres  in  the  middle 
peduncle  connect  Deiters'  nucleus  with  the  vermis  and  the  correspond- 
ing side  of  the  cerebellar  cortex  in  the  region  of  the  flocculus,  convey- 
ing impulses  to  the  cerebellum  from  the  semicircular  canals. 

The  cerebello-fugal  fibres  are  derived,  not  from  the  cortex  but  from 
the  intra-cerebellar  nuclei.  The  cerebello-fugal  fibres  of  the  superior 
peduncle,  arising  from  the  corpus  dentatum  (or  nucleus  lateralis)  run 


Nucleus  Tecii 
/NucVeiis  Glotosufe 
/    /Nucleus  Ewboliformis 
Nucleus  Dental'as 


Fig.  19. — Horizontal  section  through  cerebellum. 


upwards,  ventral  to  the  corpora  quadrigemina,  across  the  middle  line 
to  the  red  nucleus  in  the  crus  cerebri  of  the  contra-lateral  side  (Fig.  20). 
Starting  again  from  this  station,  fibres  run  forwards  along  the  anterior 
limb  of  the  internal  capsule  and  pass  to  the  optic  thalamus  and  frontal 
cortex.     This  constitutes  a  crossed  cerebello-frontal  path. 

A  small  number  of  cerebello-fugal  fibres  also  run  in  the  middle 
peduncle,  from  the  corpus  dentatum  to  the  contra-lateral  pontine 
nuclei  (formatio  reticularis),  whence  new  fibres  arise  and,  passing 
upwards  through  the  crus  cerebri  and  internal  capsule,  reach  the 
frontal,  temporal,  and  occipital  cortex.  From  the  nucleus  fastigii 
(roof  nucleus  or  nucleus  medialis)  the  fastigio-bulbar  tract,  containing 
both  crossed  and  uncrossed  cerebello-fugal  fibres,  winds  around  the 
crus  cerebri  and  reaches  to  the  vestibular  nucleus,  also  to  Deiters' 
nucleus  and  to  most  of  the  sensory  bulbar  nuclei.     The  precise  con- 


ANATOMY  AND    PHYSIOLOGY 


27 


nections  of  the  other  intra-cerebellar  nuclei  (nuclei  emboliformes  and 
nucleus  globosus)  are  not  yet  completely  identified. 


3PINALC0RD 


Fig.  20. — Cerebello-petal  and  cerebello-fugal  paths. 

It  should  be  particularly  noted  that  there  are  no  cerebello-fugal 
paths  leading  directly  downwards  to  the  spinal  cord,  but  only  indirect 
descending  paths,  one  via  the  red  nucleus  and  the  rubro-spinal  tract, 


28  NERVOUS    DISEASES 

and  another  via  Deiters'  nucleus  and  the  vestibulo-spinal  (Deitero- 
spinal)  tract. 

It  will  also  be  observed  that,  broadly  speaking,  each  lateral  half 
of  the  cerebellum  is  in  connection  (1)  mainly  with  the  cerebral  hemi- 
sphere and  pontine  nuclei  of  the  opposite  or  contra-lateral  side,  (2) 
with  both  sides  of  the  medulla,  and  (3)  with  the  same  or  ipso-lateral 
side  of  the  spinal  cord. 

Thus  the  cerebellum  receives  impulses  from  various  sources  : — 
(1)  from  the  cerebrum  through  the  superior  peduncles;  (2)  from  the 
skin,  joints,  and  muscles  through  the  inferior  peduncles ;  and  (3)  from 
most  of  the  cranial  nerve  nuclei  through  the  middle  peduncles,  especially 
from  the  semicircular  canals,  by  the  vestibular  nerve.  And  in  turn 
the  intra-cerebellar  nuclei  send  efierent  impulses  along  the  superior 
peduncles  to  the  cerebrum,  reinforcing  the  general  muscular  tonus  and 
co-ordinating  the  motor  impulses  proceeding  from  the  cerebrum. 

In  most  voluntary  movements  the  centre  of  gravity  of  the  body 
requires  to  be  altered  and  certain  muscular  groups  have  to  co-ordinate 
to  maintain  equilibrium.  For  this  purpose  the  tonus  of  these  muscular 
groups  has  to  be  augmented,  and  this  is  accomplished  by  the  cere- 
bellum, the  great  centre  for  co-ordination  and  equilibration,  partly  by 
the  action  of  the  dentate,  roof,  and  emboliform  nuclei  on  the  red 
nuclei  and  cerebral  motor  cortex ;  partly  by  the  nuclei  of  Deiters  and 
the  descending  vestibulo-spinal  tracts  to  the  spinal  cord. 

Whilst  the  cerebellum  may  be  regarded  as  the  organ  for  the 
sub-conscious  regulation  of  co-ordinated  movements  of  the  limbs 
and  trunk,  the  functions  of  the  cerebellar  cortex  differ  essentially 
from  those  of  the  intra-cerebellar  nuclei.  Clark  ^  and  Horsley 
have  shown  that  although  the  cerebellum  as  a  whole — comprising 
cortex  and  nuclei — responds  to  stimulation,  the  cerebellar  cortex 
is  relatively  insensitive  to  electrical  stimuli.  On  the  other  hand 
the  subjacent  intra-cerebellar  nuclei,  with  their  cerebello-fugal 
fibres,  can  readily  be  stimulated,  giving  rise  to  various  charac- 
teristic movements.  Nevertheless  destruction  of  localised  areas  of 
the  cerebellar  cortex  itself,  as  shown  by  the  experimental  re- 
searches of  v.  Rynbeck,  Rothmann,  and  others,  demonstrates  the 
existence  of  definite  cortical  co-ordination-centres  corresponding 
with  various  muscle-groups  of  the  limbs,  head,  and  trunk.  The 
following  CO -ordination- centres  have  been  identified  in  the  dog  by 
means  of  localised  extirpations  : — 

In  the  anterior  lobe  there  are  centres  for  the  muscles  inner- 
vated by  the  motor  cranial  nerves  (ocular,  masticatory,  facial, 
and  tongue  muscles),   and  in  the  anterior  and  posterior  lunate 

1  Brain,  1908,  p.  45. 


ANATOMY   AND   PHYSIOLOGY  29 

lobules  a  centre  for  the  neck  muscles.  Both  of  these  centres  are 
close  to  the  middle  line.  In  the  lateral  lobe  there  is  a  centre  for 
the  muscles  of  the  ipso-lateral  Umbs,  the  upper  Umb  being  farther 
forward  (in  the  lunate  lobule),  the  lower  limb  more  posteriorly  (in 
the  lobulus  semilunaris  superior).  In  the  upper  portion  of  the 
posterior  median  lobe  (inferior  vermis)  is  a  centre  for  the  muscles 
of  the  limbs  of  both  sides,  whilst  the  remainder  of  the  cerebellar 
cortex  corresponds  to  the  trunk  muscles. 

These  views  have  also  been  confirmed  by  Barany's  observations 
on  the  human  brain,  Bdrany,  by  the  temporary  freezing  of  small 
areas  of  cerebellar  cortex,  exposed  m  man  during  operation,  produces 
transient  and  localised  loss  of  function  in  these  areas.  To  identify 
them  clinically  he  employs  what  we  may  call  the  "  target "  or 
pointing  tests.  A  normal  individual,  with  closed  eyes,  can,  with 
any  of  his  limbs,  come  back  accurately  to  a  given  mark.  Never- 
theless, even  in  him  we  can  produce  an  artificial  vestibular  devia- 
tion or  mis-pointing  ("  vorbei-zeigen ")  of  all  the  hmbs  by 
inducing  vestibular  nystagmus.  (See  later.  Vestibular  Ataxia.)  In 
localised  disease  of  the  cerebellar  cortex,  however,  without  pro- 
voking any  artificial  vestibular  nystagmus,  we  have  a  spontaneous 
"  vorbei-zeigen  "  or  mis-pointing  of  the  ipso-lateral  Hmbs  only,  and 
in  a  special  direction  in  each  case,  corresponding  with  the  area  of 
cerebellar  cortex  affected. 

Btirany  maintains  the  existence  in  each  cerebellar  hemisphere 
of  four  cortical  centres  for  muscular  tonus,  viz.  for  movements 
outwards,  inwards,  upwards,  and  downwards.  Thus  in  the  right 
cerebellar  hemisphere  the  centre  for  movement  of  the  right  arm  to 
the  right  {outward  tonus)  is  beheved  by  Bartiny  to  be  near  the 
outer  edge  of  the  lateral  lobe  at  the  back  (in  the  region  of  the 
superior  and  inferior  semilunar  lobules).  When  this  centre  is 
paralysed,  the  intact  centre  in  the  opposite  side  of  the  cerebellum 
is  unopposed  and  there  is  failure  of  outward-tonus  in  the  right 
arm  only  ;  with  that  Kmb  therefore  the  patient  shows  spontaneous 
"  vorbei-zeigen  "  or  mis-pointing  towards  the  left.  The  centre  for 
movement  of  the  right  arm  towards  the  left  [inward  tonus)  whose 
paralysis  produces  spontaneous  "  vorbei-zeigen  "  of  the  arm  out- 
wards, towards  the  right,  is  on  the  anterior  aspect  of  the  right 
lateral  lobe,  in  the  region  of  the  biventral  lobule,  i.e.  close  behind 
the  bony  labyrinth  itself.  The  centre  for  downward  tonus  of  the 
upper  limb  is  near  the  postero-mesial  end  of  the  superior  and  inferior 


30  NERVOUS    DISEASES 

semilunar  lobules.  Paralysis  of  this  centre  produces  spontaneous 
mis-pointing  of  the  ipso-lateral  arm  upwards.  The  position  of  the 
centre  for  wpward  tonus  of  the  upper  limb  is  not  yet  determined. 
Similar  centres  also  exist  for  the  lower  hmbs,  of  which  that  for 
inward  tonus  has  been  identified  on  the  outer  surface  of  the  cere- 
bellar hemisphere,  behind  the  inward  tonus  arm-centre.  The 
foregoing  phenomena  are  best  seen  in  recent  or  acute  lesions.  In 
old-standing  lesions  they  are  less  distinct,  probably  owing  to 
compensation  by  the  cerebrum. 

Further,  in  cortical  cerebellar  lesions,  in  addition  to  the  spon- 
taneous mis-pointing  above  described,  we  observe  loss  of  the  normal 
vestibular  deviation  in  the  corresponding  limb,  when  we  induce  a 
vestibular  nystagmus  (see  later,  p.  146). 

Experimental  destruction  of  the  right  half  of  the  cerebellum, 
by  leaving  unopposed  the  tonic  action  of  the  other  half,  causes  the 
animal  to  rotate  around  its  own  long  axis  in  the  direction  of 
screwing  in  a  screw  (the  animal's  head  representing  the  head  of 
the  screw).  Together  with  this  rotatory  lurching,  there  is  asynergia 
of  the  ipso-lateral  arm  and  leg,  together  with  various  ocular  pheno- 
mena, including  nystagmus  owing  to  interruption  of  cerebellar 
control  over  the  ocular  nuclei  through  Deiters'  nucleus. 

Destruction  of  the  anterior  part  of  the  vermis  causes  the  animal 
to  fall  forwards,  whilst  if  the  posterior  part  of  the  vermis  be 
destroyed  the  animal  tends  to  fall  backwards. 

The  results  of  cerebellar  stimulation  are  somewhat  difficult  to 
interpret,  owing  to  the  relatively  high  excitabihty  of  the  sub- 
cortical nuclei  as  compared  with  the  cerebellar  cortex,  and  partly 
also  to  the  difficulty  of  being  sure  that  a  stimulus,  even  when 
reaching  a  particular  nucleus,  is  confined  to  it  and  not  diffused 
into  adjacent  tracts.  Horsley  and  Clark,^  however,  describe 
stimulation  of  the  upper  part  of  the  nucleus  dentatus  as  producing 
deviation  of  the  eyes  and  head  towards  the  ipso-lateral  side. 
Stimulation  of  the  basal  portion  of  the  nucleus  dentatus,  and  of  the 
upper  portion  of  the  para- cerebellar  nuclei  on  the  same  side,  pro- 
duces flexion  of  the  ipso-lateral  elbow  ;  whilst  stimulation  of  the 
para- cerebellar  nuclei  alone,  produces  tonic  extension  of  the 
contra-lateral  elbow  with  hyper-extension  of  the  neck  and  head 
and  extension  of  both  legs,  a  condition  which  closely  resembles 
certain  so-called  "  cerebellar  fits  "  in  man. 

1  Brain,  1908,  p.  45. 


ANATOMY    AND    PHYSIOLOGY  31 

Luciani,  on  experimental  grounds,  considered  asthenia  and 
muscular  atonia  as  essential  symptoms  of  cerebellar  disease.  But 
as  regards  asthenia,  cHnical  observations  do  not  show  any  true 
muscular  enfeeblement.  On  the  contrary,  the  cerebellar  patient 
has  normal  muscular  power  but  he  misapplies  it  and  uses  it 
clumsily.  With  regard  to  the  atonia  or  hypotonia,  this  is  some- 
times said  to  be  present  (although  far  from  constant),  tending,  in 
unilateral  cases,  to  be  more  marked  in  the  ipso-lateral  limbs.  It  is 
recognised  by  the  presence  of  abnormal  muscular  flaccidity  and  by 
the  readiness  with  which  the  affected  hmbs  may  be  placed  passively 
in  abnormal  postures. 

Cerebellar  catalepsy  or  excessive  static  equiUbrium,  originally 
described  by  Babinski,  consists  in  the  fact  that  the  cerebellar 
patient  can  maintain  his  limbs  immobile  in  certain  fixed  positions 
with  greater  steadiness  than  a  normal  individual.  This  is  best 
demonstrated  by  making  the  patient  lie  on  his  back  with  the  hips 
and  knees  flexed  and  then  asking  him  to  raise  his  feet  from  the 
couch  and  hold  them  in  the  air  without  touching  each  other.  During 
the  process  of  assuming  this  posture,  the  hmbs  and  trunk  show 
an  initial  hypermetria  and  asynergia,  but  in  a  few  moments  the 
hmbs  become  immobile  and  remain  fixed,  without  fatigue,  for  a 
number  of  minutes,  showing  none  of  the  oscillations  observed  in 
healthy  persons.  In  unilateral  cerebellar  disease  the  outstretched 
upper  limb  on  the  ipso-lateral  side  is  often  steadier  than  on  the 
healthy  side. 

The  pituitary  gland  is  a  small  oval  body  whose  longest  diameter 
lies  transversely.  It  occupies  the  sella  turcica  of  the  sphenoid  bone, 
being  enclosed  within  a  special  covering  of  dura  mater,  and  is 
connected  with  the  floor  of  the  third  ventricle  by  a  narrow,  hollow 
stalk — the  infundibulum,  which  leads  upwards  through  a  special 
aperture  in  the  dura.  The  pituitary  gland  consists  of  two  lobes, 
serving  different  functions : — (1)  a  larger  anterior  lobe,  purely 
epithelial  and  glandular  in  structure  and  containing  many  chromo- 
phile  cells  of  active,  secreting  nature ;  (2)  a  smaller  posterior  lobe 
which  is  subdivided  into  a  pars  intermedia,  epithelial  in  structure, 
but  without  chromophile  cells  and  a  pars  nervosa,  the  continuation 
of  the  infundibulum,  and  consisting  of  ependymal  and  neuroglial 
cells.  The  pars  nervosa  is  developed  by  outgrowth  from  the 
primitive  brain,  whereas  the  pars  intermedia  and  anterior  lobe 
are  developed  as  a  backward  diverticulum  from  the  primitive 


32  NEKVOUS    DISEASES 

ectoderm  of  the  pharynx.  In  fact,  a  smaU  longitudinal  patch  of 
pituitary  tissue  often  persists  in  the  submucous  tissue  of  the 
pharyngeal  roof,  outside  the  cranial  cavity.  ^ 

The  secretion  of  the  anterior  lobe,  which  is  related  to  the  general 
growth  of  the  body  and  especially  of  the  skeleton,  enters  the  blood- 
stream of  the  venous  sinuses  around  the  gland. 

The  secretion  of  the  pars  intermedia  and  pars  nervosa,  which 
is  of  a  colloid  character,  passes  directly  between  the  ependymal 
cells  into  the  cerebro- spinal  fluid  of  the  third  ventricle,  and  thence 
enters  the  blood-stream,  vid  the  dural  sinuses.  The  secretion  of 
this  posterior  lobe  has  a  marked  effect  in  raising  the  general  vascular 
pressure,  in  producing  contraction  in  all  varieties  of  non-striped 
muscle  {e.g.  uterus,  bladder,  intestine,  &c.),  and  also  acts  as  a  power- 
ful diuretic  and  galactogogue.  Experimental  removal  of  a  portion 
of  the  pituitary  (total  removal  is  fatal)  produces  a  remarkable  effect 
upon  the  metaboUsm  of  sugar,  causing  an  increased  power  of 
retaining  sugar  in  the  body.  In  a  normal  person,  if  more  than 
a  certain  amount  of  glucose  (about  100  grammes)  be  taken  at  a 
dose,  some  of  it  will  overflow  in  the  urine,  producing  a  temporary 
glycosuria.  But  if  the  posterior  lobe  of  the  pituitary  body  be 
destroyed,  far  larger  doses  can  be  taken  without  causing  overflow 
glycosuria. 

The  pituitary  gland  undergoes  temporary  enlargement  during 
pregnancy,  chiefly  owing  to  an  increase  in  the  chromophile  cells  of 
its  anterior  lobe.  This  enlargement  may  even  produce  hemi- 
anopia  in  pregnant  women ;  transient  acromegaly  has  also  been 
described,^  whilst  glycosuria  has  been  frequently  noted,  probably 
resulting  from  hyper- activity  of  the  posterior  lobe. 

The  pineal  gland  (conarium  or  epiphysis  cerebri)  is  a  small 
oval  body  lying  mesially  in  the  depression  on  the  dorsal  aspect  of 
the  superior  corpora  quadrigemina.  It  possesses  a  small  cavity, 
continuous  anteriorly  with  the  third  ventricle.  Involution  of  the 
gland  begins  normally  in  childhood  at  about  the  age  of  seven  years, 
and  is  complete  at  puberty.  In  the  adult  brain  the  gland  has 
already  undergone  secondary  calcareous  degeneration,  and  particles 
of  "brain-sand"  are  scattered  throughout  its  substance.  The 
pineal  gland  was  formerly  regarded  mainly  as  a  "  vestigial  "  organ, 
a  portion  of  which,  in  some  reptiles,  develops  into  a  rudimentary 

1  Civalleri,  Giornale  delV  Accademia  di  Torino,  1907. 
Haberfeld,  Ziegler's  Beitrdge  ziir  path.  Anat.,  1909,  xlvi. 

2  Marek,  Gynah.  Centralhlatt,  19II,  s.  1612, 


ANATOMY    AND    PHYSIOLOGY  33 

pineal  eye.  More  recent  observations,  however,^  show  that,  prior 
to  the  age  of  puberty  at  least,  the  pineal  gland  is  an  important 
organ  of  internal  secretion. 

The  pineal  secretion  has  a  profound  influence  upon  growth 
and  upon  certain  trophic  functions.  It  inhibits  development  of 
the  genital  glands.  Increased  secretion,  super-pinealism,  causes 
excessive  adiposity  and  retards  the  onset  of  puberty,  whereas 
diminished  secretion,  sub-pinealism  (as  in  certain  teratomata  of 
the  gland  occurring  during  childhood),  causes  precocious  and 
abnormal  development  of  the  male  genital  organs  and  also  of 
secondary  sexual  characteristics. 

1  Miinzer,  Berlin.  Klin.  Wcchensch.,  1911,  No.  37. 
Kidd,  Bev.  of  Neurol,  and  Bsych.,  1913,  pp.  1  and  55. 


CHAPTER   II 

ANATOMY   AND   PHYSIOLOGY  (mitimted) 

Having  considered  the  chief  motor  and  sensory  tracts  within  the 
central  nervous  system,  let  us  now  pass  to  the  peripheral  paths 
whereby  the  central  nervous  system  is  connected  with  the  various 
end- organs. 

Firstly,  as  to  the  motor  system.  Motor  fibres  starting  in  the 
cortex,  and  passing  down  the  pyramidal  tract,  as  already  described, 
reach  the  nuclei  of  the  various  motor  cranial  nerves  in  the  crura, 
pons,  and  medulla.  Then,  passing  along  the  spinal  cord,  the 
pyramidal  tract  gives  off  fibres  to  the  anterior  cornua  at  various 
levels  all  the  way  down.  This  portion  of  the  motor  tract,  from  the 
motor  cortex  to  the  extremity  of  the  pyramidal  fibres,  is  called 
the  upper  motor  neurone,  and  if  the  cortical  motor  cell  or  its  axon, 
the  pjrramidal  motor  fibre,  be  destroyed,  we  have  degeneration 
of  the  whole  length  of  the  pyramidal  fibre  below  the  level  of 
the  lesion,  stopping  short  when  it  reaches  the  anterior  cornual 
cell.  This  so-called  "  descending  degeneration  "  does  not,  as  the 
name  might  suggest,  begin  at  the  lesion  and  spread  downwards, 
but  affects  simultaneously  the  whole  motor  fibre  below  the  lesion, 
on  the  side  remote  from  the  nerve-cell  which  is  its  trophic  centre. 

From  each  anterior  cornual  cell  a  new  motor  fibre  passes  out 
of  the  cord  along  an  anterior  nerve-root,  enters  into  the  formation 
of  a  peripheral  motor  nerve,  and  thereby  is  conducted  to  a 
muscle-fibre.  This  lower  segment  of  the  motor  path,  starting  at 
the  anterior  cornual  cell  and  ending  in  the  muscle-fibre,  is  called 
the  lower  motor  neurone.  Here  also,  if  the  anterior  cornual  cell  or 
its  axon,  the  peripheral  motor  nerve,  be  destroyed,  we  again  have 
a  "  descending  degeneration  "  of  the  whole  fibre  on  the  distal  side 
of  the  point  of  injury,  and  of  the  muscle-fibre  also.  We  note  that 
degeneration  of  the  upper  motor  neurone  does  not  spread  into  the 
lower  neurone,  nor  vice  versa.  It  is  particularly  to  be  remembered 
that  a  lesion  of  the  upper  motor  neurone  leaves  the  lower  reflex 

34 


ANATOMY    AND    PHYSIOLOGY  35 

arc  intact,  whilst  a  lesion  of  the  lower  motor  neurone  not  only 
severs  the  reflex  arc,  but  also  causes  the  muscle-fibre  in  that  reflex 
arc  to  degenerate  and  waste  away. 

Therefore  in  diagnosing  the  position  of  the  lesion,  in  any  given 
case  of  motor  paralysis  due  to  organic  disease,  the  first  question 
we  must  ask  ourselves  is  whether  the  lesion  is  in  the  upper  (cortico- 
spinal) or  in  the  lower  (spino-muscular)  motor  neurone.  There 
is  usually  little  difiiculty  in  answering  this  question,  if  we  bear  the 
following  points  in  mind  : — 

Lesion  of  Upper  (Cortico-Spinal)      Lesion  of  Lower  (Spino-muscular) 
Motor  Neurone.  Motor  Neurone. 

1.  Motor  Paralysis.  1.  Motor  Paralysis. 

2.  Spasticity.  2.  Flaccidity. 

3.  No    muscular    wasting    (apart  3.  Muscular  Atrophy. 

from  disuse). 

4.  Electrical  reactions  normal.  4.  R.D.  (reactions  of  degeneration). 

5.  Deep  reflexes  present  and  often  5.  Deep  reflexes   absent  or  dimi- 

increased.  nished. 

6.  Extensor  plantar  reflex  (if  leg  6.  Plantar    reflex,    if    present,    of 

affected).  normal   flexor  type  (unless 

lesion       jjaralyses       flexor 
muscles  themselves). 

Having  thus  recognised  which  motor  neurone,  upper  or  lower,  is 
affected,  we  have  then  to  decide  at  what  level  in  the  affected  neurone 
the  lesion  is  situated.     To  that  point  we  shall  come  later. 

Returning  for  a  moment  to  the  sensory  fibres ;  these  may 
also  be  regarded  as  arranged  in  sensory  neurones.  The  lowest 
sensory  neurone  starts  from  a  sensory  end- organ,  in  the  skin  or 
elsewhere,  and  extends  up  to  the  nerve-cell  in  the  intervertebral 
ganglion  on  the  posterior  spinal  root.  This  ganglion-cell  is  the 
trophic  centre  for  the  peripheral  sensory  fibre,  and  a  lesion  at  or 
below  this  cell  will  cause  "  descending  degeneration  "  of  the  distal 
segment  of  the  fibre  and  of  the  peripheral  end-organ.  There  is, 
however,  one  sensory  end-organ,  the  muscle-spindle,  which  is  an 
exception  to  this  rule,  and  does  not  degenerate  when  the  afferent 
fibre  leading  from  it  to  the  ganglion-cell  is  destroyed.  The 
muscle-spindle  thus  has  its  trophic  centre  within  itself. 

But  the  ganglion-cell  of  the  posterior  root  is  also  the  trophic 
centre  for  the  fibre  which  passes  upwards  from  it  along  the  pos- 
terior root  and  enters  the  posterior  column  of  the  spinal  cord. 
And  therefore  a  lesion  at  or  above  the  intervertebral  ganglion-cell, 
in  the  posterior  root,  or  in  its  intra-spinal  prolongation  in  the  pos- 


36  NERVOUS    DISEASES 

terior  column,  will  cause  an  "  ascending  degeneration  "  of  the  fibre 
through  its  whole  course  within  the  spinal  cord.  Here  again  this  so- 
called  "  ascending  "  degeneration  occurs  simultaneously  throughout 
the  entire  extent  of  the  nerve-fibre,  on  the  side  remote  from  its 
trophic  centre  in  the  intervertebral  ganglion  ;  and  this  degeneration 
extends  as  far  as,  but  does  not  iraphcate,  the  next  nerve-cell  whose 
axon  leads  upwards  towards  the  brain.  Similarly  a  lesion  of  this 
second  sensory  neurone  causes  ascending  degeneration  in  the  fibre 
of  the  fillet  above,  as  far  as,  but  not  including,  the  optic  thalamus. 
There  a  third  neurone  starts,  leading  up  to  the  sensory  area  of  the 
cerebral  cortex.  In  the  case  of  the  ordinary  sensory  tract,  the 
path  traverses  the  internal  capsule. 

In  the  case  of  an  impulse  which  traverses  the  cerebellum, 
the  chain  of  successive  neurones  is  more  complex,  and  consists 
of  (1)  a  posterior-root  neurone,  (2)  an  ascending  spino-cerebellar 
neurone,  (3)  a  cerebello-dentate,  (4)  a  dentato-thalamic,  and  (5)  a 
thalamo- cortical  neurone. 

The  so-called  "  Wallerian  degeneration  " — "  ascending  "  or 
"  descending  "  as  the  case  may  be — signifies  that  a  nerve-fibre, 
separated  from  its  trophic  cell,  degenerates  on  the  side  remote 
from  that  cell.  It  should  also  be  remembered  that  after  lesions 
of  a  cranial  or  spinal  nerve,  especially  in  a  young  animal,  marked 
chromatolytic  changes  are  produced  in  the  nerve  cells  of  the 
corresponding  motor  nucleus  in  the  bulb  or  spinal  cord. 

The  anterior  and  posterior  nerve-roots  join  to  form  mixed 
nerve-trunks.  These  again  branch  and  intermingle  to  form  plexuses 
in  the  cervical,  lumbar,  and  sacral  regions.  The  distribution 
of  the  different  nerves,  motor  and  sensory,  is  represented  in 
Figs.  21,  22,  and  23. 

Root  Lesions. — But  what  is  perhaps  less  familiar,  though  of 
equal  diagnostic  importance,  is  the  distribution  of  the  anterior 
and  posterior  spinal  roots.  In  lesions  of  the  lower  motor  neurone, 
we  have  often  to  decide  whether  the  distribution  of  symptoms 
points  to  a  lesion  of  a  peripheral  nerve-trunk,  such  as  the 
musculo-spiral  or  sciatic,  or  whether  it  points  to  a  lesion  of 
one  or  more  nerve-roots  before  they  have  joined  to  form  the 
trunks  of  a  plexus.  Thus,  for  example,  the  deltoid  is  fre- 
quently paralysed  alone  owing  to  a  lesion  of  the  circumflex 
nerve,  but  it  is  never  paralysed  alone  as  a  result  of  a  lesion 
of     the    anterior     cornu     or    anterior     nerve-root.        Again,     a 


ANATOMY    AND    PHYSIOLOGY 


37 


lesion  of  the  musculo  -  spiral 
nerve  may  produce  paralysis 
both'  of  the  supinator  longus 
and  of  the  extensors  of  the  wrist 
and  fingers,  but  these  muscles 
are  never  affected  together  by 
a  lesion  of  a  single  segment 
of  the  spinal  cord  or  of  a 
single  anterior  root,  since  their 
motor  cells  lie  at  different 
levels  in  the  anterior  cornu. 
This  will  be  readily  seen  on 
studying  the  tables  on  p.  41, 
which  show  the  nuclear  re- 
presentation of  muscles  in  the 
anterior  cornua  at  various  levels 
of  the  spinal  cord.  For  clinical 
purposes,  the  distribution  of 
each  anterior  root  may 
be  considered  to*  be  the 
same  as  that  of  the  spinal 
segment  from  which  it 
arises. 

In  connection  with  'the 


38 


NERVOUS   DISEASES 


root  distribution  of  sensory  and  motor  fibres,  it  is  interesting 
to  note  that  in  eacli  embryonic  segment  or  metamere,  the  mus- 
cular territory  (myotome)  of  the  segment  corresponds  more  or 
less   closely   with  the   cutaneous    distribution    (dermatome)    and 


w 


with  a  zone  of  the  bony  skeleton  (sclerotome).  In  the  trunk 
this  segmental  or  metameric  arrangement  is  comparatively  easy 
to  recognise,  especiall)^  in  the  thorax ;  and  even  in  the  limbs 
a  similar  arrangement,  though  more  complex,  can  be  made  out. 


ANATOMY    AND    PHYSIOLOGY 


39 


40 


NERVOUS   DISEASES 


Thus,  as  Bolk  has  shown,  in  the  limbs  there  is  for  every  spinal 
segment  a  corresponding  dermatome,  myotome,  and  sclerotome, 
but  they  are  subdivided  into  a  pre -axial  and  a  post-axial  division 
in  each  case  (see  Fig.  24). 

We  observe  that  comparatively  few  muscles  are  confined  to  a 
single  segment,  but  that  most  of  them  are  represented  in  two  or 
more  segments.  If,  therefore,  a  cord  lesion  be  limited  to  one 
segment,  it  will  cause  complete  paralysis  of  the  muscles  ccm- 
fined  to  that  particular  segment  and  partial  paralysis  of  muscles 
whose  motor  nuclei  extend  up  or  down  into  other  segments.     This 


Sy   \  ^z  V       S 


Fig.  24. — Transversa  section  through  upper  third  of  thigh. 
The  thick  black  line  indicates  the  boundary  between  the 
pre-axial  and  post-axial  regions  of  the  hmb.  The  fine  black 
lines  mark  the  segmental  distribution.     (After  Bolk.) 


explains  the  apparent  irregularity  in  the  distribution  and  degree 
of  paralysis  in  certain  cases  of  infantile  paralysis  and  other  diseases 
of  the  anterior  horns. 

Similarly  in  a  case  of  cutaneous  ansesthesia  it  is  important 
to  distinguish  between  a  posterior-root  lesion  and  a  lesion  of  a 
peripheral  nerve-trunk  such  as  the  radial  or  ulnar.  The  dis- 
tribution of  the  posterior  nerve-roots  is  indicated  diagrammati- 
cally  in  Figs.  25  and  26. 

It  is  sometimes  difl&cult  for  the  student  to  remember  the  arrange- 
ment of  these  cutaneous  root-areas,  since  in  the  trunk  they  run 
mainly  horizontally,  whereas  in  the  upper  limbs  they  run  longitudinally, 
parallel  to  the  axis  of  the  limb,  whilst  in  the  lower  limbs,  anteriorly, 
they  run  from  above  downwards,  and  posteriorly,  from  below  upwards. 
Finally  the  genital  organs,  innervated  by  the  third  and  fourth  sacral 


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luc. 

O 

Lumbo-Sacral   Cord 

Lumbric 

Inteross 

ales 
ei 

Ph 

Sphincter  An 

i  exter. 

Le 

vator 

Ani 

Per 

ineal 

Muscles 

42 


NEEVOUS    DISEASES 


Fig.  25. — Diagram  of  Cutaneous  Areas  of  Posterior  Roots.    (After  Collier  and 

Purves  Stewart.) 


roots,  are  suspended,  as  it 
were,  amongst  strangers, 
viz.  in  the  neighbourhood 
of  the  second  and  third 
lumbar  areas  (see  Fig. 
25). 

The  teaching  of  these 
areas  can  be  simplified  as 
follows  : — Let  us  regard 
the  body  as  a  long  cylin- 
der, beginning  above  at 
the  head,  innervated  by 
the  trigeminal  nerve,  and 
ending  below  at  the 
coccyx.     If  this  body  had 


Fig.  26. — Sacro-coccygeal  Root-areas. 


ANATOMY    AND    PHYSIOLOGY 


43 


no  limbs,  everything  would  be  easy,  and  we  might  represent  the 
various  root-areas  as  a  series  of  horizontal  dermatomes  running 
from  above  downwards,  with  the  nose  and  mouth  in  the  tri- 
geminal area,  the  nipples  at  the  junction  of  the  fifth  and  sixth 
thoracic,  the  umbilicus  at  the  junction  of  the  ninth  and  tenth  thoracic, 
and  the  anus  within  the  fourth  sacral  area  (Fig.  27a).  The  upper 
extremities^  growing  outwards  horizontally  from  the  trunk  in  the 
cervico-thoracic  region,  carry  with  them  the  corresponding  root-areas, 
which  run  m  long  strips  parallel  to  the  long  axis  of  the  limbs,  the 
thumbs  being  directed  upwards  (Fig.  27b).  In  the  fully  developed 
condition  these  areas  on  the  trunk  are  reduced  to  a  mere  line,  so  that 
the  fourth  cervical  segment  comes  to  touch  the  third  thoracic  segment. 


2  r 

3 
4- 

5 

^ 

6 

— '-i 

-rr^ 

8 

—y 

2 
3 

7 

8 

12 
1 
2 

r 

^ 

3 
4 

^ 

\ ^"^ 

w/ 

Fig.  27A. 


Fig.  27b. 


The  lower  limbs  may  also  be  represented  as  horizontal  outgrowths 
in  the  lumbo-sacral  region,  being  strongly  rotated  from  within  out- 
wards, so  as  to  place  the  great  toes  uppermost.  In  this  position  the 
cutaneous  root-areas  run  from  above  downwards,  the  pre-axial  roots 
running  along  the  anterior  aspect  and  the  post-axial  roots  along  the 
posterior  aspect,  always  from  above  downwards.  It  is  essential  in 
this  scheme  to  retain  a  small  projecting  tail  with  the  lower  sacro- 
coccygeal root-areas.  In  the  fully  developed  condition  this  tail,  of 
course,  is  embedded  in  the  posterior  wall  of  the  anus.  Finally,  the 
genital  organs,  innervated  by  the  third  and  fourth  sacral  roots,  are 
inclined  forwards. 

Plate  I.  is  from  a  coloured  model,  constructed  according  to  the 
foregoing  scheme,  in  which  the  various  root-areas  are  coloured  in  series 
according  to  the  order  of  the  tints  in  the  spectrum.   Thus  red  =  No.  1, 


44 


NERVOUS   DISEASES 


orange  =  No.  2,  yellow  =  No.  3,  green  =  No.  4,  blue  =  No.  5,  indigo 
=  No.  6,  violet- No.  7,  and  brown  =  No.  8.  Nos.  9  to  12  are  indi- 
cated by  paler  shades  of  blue,  indigo,  violet,  and  brown  respectively. 
Lastly,  on  one  side  of  the  model  we  have  also  indicated  the  areas  of 
distribution  of  the  various  peripheral  nerves,  for  purposes  of  comparison. 

Paths  of  Special  Senses.— Olfactory  Path. — The  olfactory 
nerves,  about  twenty  on  each  side,  arising  from  the  under  surface 
of  each  olfactory  bulb,  perforate  the  cribriform  plate  of  the 
ethmoid  bone  and  are  distributed  to  the  olfactory  region  of  the 


Fia.  28. — Diagram  of  Connections  of  Olfactory  Nerves. 

nasal  mucous  membrane  on  the  superior  turbinal  body  and  the 
corresponding  uppermost  part  of  the  nasal  septum.  The 
central  olfactory  tract  has  various  connections,  not  of  great 
clinical  importance,  leading  to  the  optic  thalamus  and  to 
other  sub-cortical  ganglia.  It  connects  the  olfactory  bulb 
with  the  cortical  centre  for  smell,  situated,  as  we  have  already 
seen,  in  the  uncinate  gyrus  at  the  tip  of  the  temp  or  o- sphen- 
oidal lobe  (Fig.  4).  The  olfactory  tract  does  not  traverse  the 
internal  capsule.  Each  olfactory  bulb  is  connected  not  only 
with  the  uncinate  gyrus  of  the  same  side,  but  also,  through  the 
anterior  commissure,  with  that  of  the  opposite  side.  (See 
Pig.  28.) 


PLATE     I. 


COLOURED     MODEL     SHOWING     CUTANEOUS     ROOT-AREAS. 


Peripheral-Nerve  Areas  are  indicated,  by  white  lines,  on  the 
right  half  of  the  model. 


[7"o  face  p.  42. 


ANATOMY    AND    PHYSIOLOGY  45 

Visual  Path. — This  is  of  great  clinical  importance.  Starting 
from  the  retina,  the  visual  fibres  run  backwards  along  the  optic 
nerve.  At  the  optic  chiasma  there  is  a  partial  decussation,  so  that 
the  fibres  from  the  left  halves  of  both  retinae  (corresponding  to  the 
right  halves  of  the  visual  fields)  run  together  in  the  left  optic 
tract,  and  vice  versd.  The  central  visual  impulses,  from  each 
macula  lutea,  pass  into  both  optic  tracts.  The  fibres  of  each  optic 
tract  run  backwards,  winding  around  the  outer  side  of  the  crus 
cerebri,  to  the  primary  optic  centres,  viz.  the  posterior  part 
of  the  optic  thalamus,  the  external  geniculate  body,  and  the 
anterior  corpus  quadrigeminum. 

From  these  three  stations  new  fibres  arise,  forming  the  "  optic 
radiation,"  passing  through  the  internal  capsule  behind  the 
fibres  for  common  sensation  (Fig.  7)  and  so  reaching  the  cortical 
half-vision  centre.  This  centre,  mainly  on  the  mesial  aspect  of 
the  hemisphere,  is  divided  into  an  upper  and  a  lower  part  by 
the  calcarine  fissure  (Fig.  4).  Above  the  fissure  is  the  cuneate 
lobe,  below  it  is  the  lingual  gyrus.  The  half -vision  centre  also 
extends  on  to  the  convexity  of  the  occipital  lobe  at  its  posterior 
extremity  (Fig.  3).  The  calcarine  fissure  forms  a  boundary- 
line  between  the  cortical  representations  of  the  upper  and  lower 
quadrants  of  the  corresponding  half  of  the  visual  field.  Therefore 
a  lesion  of  the  left  occipital  lobe,  or  of  the  whole  of  the  left 
cuneus  and  lingual  gyrus,  or  of  the  fibres  of  the  left  optic  radiation, 
will  cause  a  right-sided  hemianopia  in  both  visual  fields  ;  a  lesion 
of  the  left  cuneus,  i.e.  limited  to  the  part  above  the  calcarine 
fissure,  will  cause  blindness  of  the  right  lower  quadrant  of  both 
visual  fields  ;  whilst  if  the  lesion  be  leloio  the  left  calcarine  fissure, 
in  the  lingual  gyrus,  it  will  produce  blindness  of  the  right  upper 
quadrant  of  both  fields.  These  are  varieties  of  "  quadrantic 
hemianopia." 

Besides  the  half-vision  centre,  there  is  a  higher  centre  on  the 
convex  surface  of  the  occipital  cortex,  where  a  lesion,  if  suffi- 
ciently superficial  (so  as  to  miss  the  subjacent  optic  radiations), 
may  cause,  not  hemianopia,  but  what  is  called  "  crossed  ambly- 
opia." This  means  a  concentric  contraction  of  both  visual  fields, 
more  marked  in  the  eye  of  the  side  opposite  to  the  side  of  the 
lesion.  Such  a  lesion  has  not  been  conclusively  demonstrated 
in  gross  organic  disease,  but  crossed  amblyopia  is  one  of  the  most 
frequent  symptoms  in  hysteria. 


46 


NERVOUS    DISEASES 


Finally,  in  right-handed  people   there  is  in  the  left  angular 
gyrus  a  centre  for  the  storage  of  visual  memories  of  written  and 


Optic  Kadiations 
Corpus  Callosum 

Optic  Thalamus 
Corp.  genie,  ext. 


Optic  Tract 


Optic  Nerve 


Visual  Word  Centre 


Auditory  Word-Centre 


Vocal  Word-Centre  i 


Fig.  29.— Diagram  of  Visual  Paths  (after  Vialet). 

Lesion  at  1      produces  Blindness  of  one  eye. 

at  2  ,,        Bi-temporal  Hemianopia. 


,,  3  and  3 

„  6 

,,  7 


Bi-nasal  Hemianopia. 
R.  Hemianopia  with  Hemiopic  Pupil  Reaction. 
,,  with  Normal  Pupil  Reaction. 

Crossed  Amblyopia. 
Word-Blindness. 


printed  speech.  If  this  centre  be  destroyed,  we  have  word-blind- 
ness, which  may  or  may  not  be  associated  with  right  hemianopia, 
according  as  the  subjacent  optic  radiations  are  affected  or  not. 


ANATOMY    AND    PHYSIOLOGY  47 

Fig.  29  indicates  diagrammatically  tliese  various  fibres  and  centres, 
and  also  shows  the  effects  upon  the  visual  fields  of  lesions  in  various 
parts  of  the  visual  path. 

Gustatory  Path. — The  course  of  the  taste-fibres  outside  the 
brain  is  somewhat  complex,  and  we  shall  study  it  again  later  when 
we  consider  the  cranial  nerves.  It  is  probable  that  some  of  the 
taste  impulses,  chiefly  those  from  the  front  of  the  tongue,  enter  the 
brain  through  the  sensory  root  of  the  fifth  cranial  nerve,  some 
through  the  glosso-pharyngeal  nerve,  and  some  through  the 
nervus  intcrmedms  or  sensory  root  of  the  facial.  The  cortical 
centre  for  taste  is  in  the  front  part  of  the  temporal  lobe,  close 
to  the  olfactory  centre  (Fig.  4).  The  intra-cerebral  course  of  the 
gustatory  fibres  is  not  definitely  settled,  but  it  is  probable  that 
they  do  not  traverse  the  internal  capsule. 

Auditory  Path. — This  is  of  some  practical  importance  (Fig.  30). 
Entering  the  medulla  in  the  cochlear  division  of  the  eighth  nerve, 
the  auditory  fibres  embrace  the  restiform  body,  some  passing 
along  its  inner  side  to  the  ventral  auditory  nucleus,  others 
passing  along  its  outer  side  to  the  dorsal  auditory  nucleus.  From 
these  two  nuclei  new  fibres  pass  upwards  towards  the  cortex. 
A  few  run  up  uncrossed  in  the  fillet  of  the  same  side,  but  most 
of  the  fibres  decussate  and  ascend  in  the  fillet  of  the  opposite 
side.  Some  end  in  the  posterior  corpus  quadrigeminum,  others 
go  on  to  the  corpus  geniculatum  mediale,  and  finally  the  bulk 
of  them,  passing  through  the  sub-lenticular  region  of  the  internal 
capsule  behind  the  sensory  fibres,  reach  the  cortical  auditory 
centre  in  the  superior  temporal  convolution  (Fig.  3),  and  in  the 
anterior  transverse  temporal  convolution  of  Heschl : — Flechsig's 
"  auditory  gyrus  "  ^  (situated  on  the  upper  surface  of  the  temporal 
lobe,  at  the  bottom  of  the  Sylvian  fossa,  immediately  behind  the 
insula),  with  which  the  superior  temporal  is  continuous.  We  note 
that  each  cortical  centre  receives  auditory  messages  from  both 
ears,  though  more  extensively  from  the  ear  of  the  opposite  side, 
and  that  therefore  a  lesion  limited  to  one  temporal  lobe  will  not 
cause  deafness.  In  right-handed  people  there  is  a  specially 
differentiated  portion  of  the  left  auditory  centre  where  memories 
of  word-sounds  are  stored  up  (Fig.  3). 

A  certain  amount    of   clinical    evidence  ^    supports    the    view 

^  Neurologisches  Centralhlatt,  1908,  p.  1. 

^  Stephen  Paget,  Essays  for  Students,  1898. 


48  NERVOUS    DISEASES 

that  there  is  a  special  cortical  centre  associated  with  the 
sensations  of  hunger  and  thirst.  It  would  appear  to  be  in 
the  temporal  lobe,  at  or  near  the  olfactory  centre.  Abscesses, 
injuries  and  tumours  in  this  region  have  been  associated 
with  voracious  appetite  and  intense  thirst,  persisting  for  weeks 
or  months. 

Arteries   of  the   Brain.— Most  cases  of  acute  brain  disease 


TEMPORAL  CORTEX 


Corp.  CiPnUuJ  e»t 
Corp,  Genicul-  mcdiaU 


Tig.  30. — Diagram  of  Connections  of  Cochlear  and  Vestibular  Nerves. 

which  we  meet  with  in  civil  practice  are  the  direct  result  of  some 
vascular  disease,  e.g.  haemorrhage,  thrombosis,  or  embolism.  It 
is  therefore  important  to  understand  certain  facts  about  the 
cerebral  circulation. 

The  brain  is  supplied  by  two  pairs  of  arteries — ^the  internal 
carotids  and  the  vertebrals,  as  shown  in  Fig.  31.  The  two 
vertebral    arteries   join  to  form    the    basilar  artery   which  runs 


ANATOMY    AND    PHYSIOLOGY 


49 


forwards  in  the  middle  line  along  the  front  of  the  pons,  supply- 
ing perforating  branches  to  the  pons  and  arteries  to  the  cere- 
bellum. Between  the  crura  cerebri  the  basilar  divides  into 
the  two  posterior  cerebral  arteries,  each  of  which  winds  round 
the  outer  side  of  the  crus,  supplying  it  as  it  passes,  and  also 
giving  branches  to  the  optic  thalamus  and  the  corpora  quadri- 
gemina.  Finally  it  reaches  and  supplies  the  lower  part  of  the 
temporo-occipital  cortex  (Figs.  .32  and  3.3).     Each  posterior  cerebral 


Anterior  cerebral 


Middle  cerebral 


Sylvian 


Posterior  cere- 
bral 


Lenticulo  optic 

Lenticulo-etriate 
set  of  arteries 

Internal  carotid 


Basilar 


Vertebral 


Fig.  31. — Arteries  at  the  base  oE  the  Brain.     One,  the  lenticulo-striate,  is 
called  the  artery  of  cerebral  hjemorrhage.     (After  Dercum.) 

artery  sends  a  posterior  communicating  artery  forwards  to  join 
the  internal  carotid. 

The  internal  carotid,  close  to  its  termination,  gives  ofE  an 
important  branch — the  anterior  choroid  artery,  which  passes 
backwards  to  enter  the  descending  horn  of  the  lateral  ventricle. 
The  area  supplied  by  the  anterior  choroid  (see  Figs.  32  and  33) 
includes  the  posterior  two -thirds  of  the  posterior  limb  of  the  in- 
ternal capsule,  part  of  the  choroid  plexus  of  the  lateral  ventricle, 
and  also  the  uncinate  gyrus  of  the  temporal  lobe.^  Finally,  the 
internal  carotid  divides  into  three  main  branches  —  anterior 
cerebral,  middle  cerebral,  and  posterior  communicating.  The  two 
anterior  cerebral  arteries  are  connected  by  the  short  anterior  com- 


Beevor,  Brain,  1907,  p.  403. 


D 


50 


NERVOUS    DISEASES 


municating  artery,  thus  completing  the  "  circle  of  Willis."  The 
anterior  cerebral  artery  passes  forward,  and  then,  curving  round 
to  the  top  of  the  corpus  callosum,  turns  backwards,  parallel 
with  its  fellow  of  the  opposite  side,  between  the  mesial  surfaces  of 
the  two  hemispheres.  Most  of  the  mesial  surface  of  the  cerebral 
hemisphere,  as  far  back  as  the  parieto-occipital  fissure,  is  supplied 
by  the  anterior  cerebral  artery  (Figs.  32  and  33).  It  also  sends 
branches  over  the  edge  of  the  hemisphere  to  its  convex  surface, 
supplying  the  anterior  and  mesial  part  of  the  frontal  lobe  and  a 


^rea,  of 
A  niervor  Cerebral 


Uu0^ 


Cere* 


Posterior  Cerehiui- 


jirea  of 
l:>5terwr  Cerebral 


1  n  terwr  Cerebral, 


AntBT-Cor  Choroid,  ^rcuu3h 
'  of  Jhternal  CaroUA. 


-Middle,  Cerebral 
Fig.  32. — Diagram  of  arterial  svipply  of  cortex. 

small  part  of  the  parietal  lobule.  And  at  the  beginning  of  its 
course,  it  sends  a  few  perforating  branches  inwards  to  the  caudate 
nucleus. 

The  middle  cerebral  artery,  or  arteria  fossce  Sylvii,  is  clinically 
the  most  important  of  the  three.  Its  main  trunk  passes  upwards 
and  outwards  along  the  Sylvian  fissure  to  the  surface  of  the  island 
of  Reil,  where  it  divides  into  its  terminal  branches.  At  its  be- 
ginning it  gives  off  numerous  basal  perforating  arteries,  which 
enter  the  anterior  perforated  space  and  ascend  to  the  caudate  and 
lenticular  nucleus  (which  together  constitute  the  corpus  striatum), 
also  to  the  optic  thalamus.     These  branches  are  called  lenticular, 


ANATOMY    AND    PHYSIOLOGY 


51 


Anterior  Cerebral/ 


Middle  CerebraL 


'-Anterior  Choroid/ 


lenticulo -striate,  and  lent iculo -optic,  according  to  their  distribu- 
tion. All  these,  and  especially  the  lenticulo-striate  arteries,  are 
frequently  the  seats  of  cerebral  hajmorrhage.  The  main  trunk 
of  the  middle  cerebral  runs  along  the  Sylvian  fissure,  where  it 
divides  into  four  terminal  branches  (Figs.  32  and  33).  One  goes 
to  Broca's  convolution  (the  third  inferior  frontal) ;  another  to 
the  lower  two -thirds  of  the  pre -central  convolution  and  to  the 
adjacent  part  of  the  second  frontal  convolution  ;  another  to  the 
post-central  convolution  and  the 
adjacent  superior  parietal  con- 
volution ;  and  a  fourth  to  the 
supra -marginal  convolution,  the 
angular  convolution  and  the 
upper  temporal  convolutions, 
and     so    to    the 

tip  of  the  lobe  on        ^osterim-Cc 

its  mesial  aspect. 

The  cortical  arteries 
anastomose  with  one 
another,  but  not  so  the 
perforating  basal  vessels. 
They  are  "  terminal  " 
arteries,  and  do  not 
anastomose  either  with 
each  other  or  with  the 
cortical  vessels.  There- 
fore if  a  basal  artery  becomes  blocked  by  thrombosis  or  em- 
bolism, a  permanent  area  of  necrosis  results.  On  the  other  hand, 
the  blocking  of  a  cortical  artery  admits  of  a  more  favourable 
prognosis,  since  a  collateral  circulation  may  develop  and  the 
necrotic  process  be  arrested. 

The  cerebellum  is  supplied  by  the  anterior  cerebellar  and 
superior  cerebellar  arteries  from  the  basilar,  and  by  the  posterior 
cerebellar  arteries  from  the  vertebral.  The  posterior  inferior 
cerebellar  artery,  which  supplies  the  lateral  aspect  of  the  medulla, 
is  of  some  clinical  importance  inasmuch  as  when  it  is  thrombosed 
the  resulting  area  of  destruction  (including  the  inferior  olive,  the 
restiform  body,  and  the  intervening  nuclei  of  the  vagus  and 
glosso-pharyngeal)  produces  a  characteristic  unilateral  bulbar 
syndrome  (see  later,  p.  275). 


IbstBTwr  Cerebral 


Fig.  33. 


-Arterial  supply  of  basal  ganglia  and 
cortex.     (After  Beevor.) 


52  NERVOUS    DISEASES 

The  spinal  cord  is  supplied  by  three  main  arteries,  one  anterior 
and  two  posterior,  running  on  the  surface  along  the  entire  extent 
of  the  cord.  The  anterior  spinal  artery  arises  from  one  or  other 
vertebral,  receiving  a  small  communicating  branch  from  the  oppo- 
site vertebral.  As  it  runs  down  the  front  of  the  cord,  it  is  reinforced 
by  a  series  of  smaller  vessels,  derived  from  the  intercostal  and 
lumbar  arteries,  which  enter  here  and  there  along  the  anterior 
roots.  The  anterior  spinal  artery  sends  numerous  branches  deeply 
along  the  pia  mater  lining  the  median  fissure,  dipping  alternately 
into  the  right  and  left  sides  of  the  fissure,  and  supplying  the 
grey  matter  of  the  cord.  The  two  posterior  spinal  arteries,  one 
on  each  side,  also  arise  from  the  vertebral  arteries  and  run 
downwards  on  the  back  of  the  cord,  close  to  the  posterior  roots, 
being  reinforced  by  small  branches  entering  here  and  there  along 
the  posterior  roots.  Fig.  34  shows  diagrammatically  the  position 
of  these  various  spinal  arteries,  and  it  should  be  observed  that  the 
grey  matter  and  the  white  receive  their  blood-supply  from  different 
vessels.  Moreover,  Hke  the  perforating  basal  arteries  of  the  brain, 
all  the  spinal  arteries,  once  they  have  penetrated  the  cord,  are 
terminal  arteries  and  do  not  anastomose.  Therefore  embolism  or 
thrombosis  of  a  spinal  artery  always  produces  an  area  of 
necrosis. 

The  Venous  Circulation  in  the  brain  is  peculiar,  inasmuch  as  the 
direction  of  the  blood-stream  in  the  cortex  is  the  same  in  the 
arteries  as  in  the  veins,  i.e.  from  before  backwards.  The  superior 
longitudinal  sinus  receives  not  only  the  superior  cerebral  veins  from 
the  cortex,  but  also  some  veins  from  the  scalp,  and  through  its 
starting-point  at  the  foramen  caecum  it  receives  branches  from  the 
nasal  vein,  though  after  childhood  this  foramen  often  becomes 
closed.  Therefore  when  thrombosis  of  the  superior  longitudinal 
sinus  occurs  in  a  marasmic  child,  we  expect  epistaxis,  convulsions, 
and  distension  of  the  nasal  veins,  together  with  distension  of  the 
veins  of  the  scalp.  Posteriorly  the  superior  longitudinal  sinus 
ends  at  the  torcular  Herophili. 

The  inferior  longitudinal  sinus  is  quite  small,  and,  like  the 
superior,  lies  between  the  layers  of  the  falx  cerebri,  but  at  its  lower 
edge.  It  runs  backwards  to  the  anterior  edge  of  the  tentorium, 
receiving  branches  from  the  mesial  surface  of  the  hemispheres,  and 
ends  in  the  straight  sinus.  The  straight  sinus  receives  some 
cerebellar  veins  and    the  veins  of  Galen  from  the  velum  inter- 


ANATOMY    AND    PHYSIOLOGY 


53 


positum  and  interior  of  the  brain,  and  passes  backwards  either  into 
the  torcular  Herophili  or  into  one  of  the  lateral  sinuses.  When 
the  veins  of  Galen  are  thrombosed  the  cerebral  ventricles  become 
distended  with  fluid. 

The  lateral  sinuses  begin  at  the  internal  occipital  protuberance 
and  arch  outwards,  one  on  each  side,  to  open  through  the  jugular 
foramen  into  the  internal  jugular  vein.  The  sinus  passes  close 
to  the  mastoid  portion  of   the  temporal  bone.      Here  it  receives 


AnJj^RouhjcuLour^ 
branches  from, a  ^^^ 
InlRrcost/xL 
Artery,  ' 


AnJJ^SpiruiL  Artery. 


Anb"^  EjOLObbcular 
. — ■~'^.  branches  rronv 
I        /     \,  Intercostnl  Artery, 
BroavcTvtc  Anterior  MidLarvFiiSS  lire 


I'ustericfr 

SpiaaL Artery- 


rPosberior 
SpinaJjArtery. 


Fig.  34. — Diagram  of  the  course  and  distribution  of  the  terminal  arteries  of 
the  spinal  cord.     (After  Van  Gehuchten.) 


the  superior  petrosal  sinus,  and  also  emissary  veins  from  the 
scalp  in  the  mastoid  region.  Just  before  it  empties  into  the 
jugular,  it  receives  the  inferior  petrosal  sinus  and  sometimes  the 
occipital  sinus  from  the  torcular.  Lateral  sinus  thrombosis  is  a 
well-known  and  dangerous  comphcation  of  suppuration  in  the 
middle  ear.  It  is  recognised  by  distension  of  the  mastoid  veins, 
oedema  of  that  region,  and  hardness  and  tenderness  of  the 
internal  jugular  vein.  Together  with  this  we  may  have  rigidity 
of  the  neck,  tinnitus,  vertigo,  and  even  signs  of  compression  of 
the  vagus,  such  as  dyspnoea,  dysphagia,  bradycardia,  and  palatal 


54 


NERVOUS    DISEASES 


paresis.  It  is  not  uncommon  to  find  swelling  and  oedema  of  the 
ipso-lateral  optic  disc.  Crowe  ^  has  pointed  out  an  additional 
physical  sign,  based  upon  the  fact  that  in  health,  if  one  internal 
jugular  vein  be  compressed  in  the  neck,  the  retinal  vessels  show 
no  change,  but  when  both  jugulars  are  digitally  compressed, 
the  retinal  veins  became  visibly  engorged.     If  one  jugular  vein 

(or  the  lateral  sinus  from  which  it 
arises)  be  already  obstructed  by  throm- 
bosis, pressure  on  the  jugular  vein 
of  the  sound  side  will  produce  venous 
engorgement  of  the  retinal  veins  (visible 
by  means  of  direct  ophthalmoscopy) 
and  sometimes  also  of  the  supra-orbital 
veins :  whereas  if  both  jugulars  are 
patent,  pressure  on  one  jugular  pro- 
duces no  such  result. 

The  cavernous  sinuses  lie  one  on 
each  side  between  the  sphenoidal  fis- 
sure and  the  apex  of  the  temporal  bone. 
Each  sinus  receives  the  ophthalmic 
veins  from  the  orbit  and  communicates 
by  means  of  the  circular  (or  inter- 
cavernous) sinus  with  its  fellow  of  the 
opposite  side.  The  sinus  ends  posteriorly  by  opening  into  the  two 
petrosal  sinuses. 

Thrombosis  of  the  cavernous  sinus  is  generally  secondary  to 
some  septic  condition  of  the  orbit,  naso-pharynx,  or  sphenoidal 
sinus.  It  is  recognised  by  the  presence  of  chemosis  (oedema  of  the 
conjunctiva),  proptosis  (bulging  forwards  of  the  eyeball),  and 
oedema  of  the  upper  lid  and  root  of  the  nose  (see  Fig.  35).  There 
may  be  paralysis  of  certain  of  the  external  ocular  muscles  from 
affection  of  the  third,  fourth,  or  sixth  nerves  which  lie  in  the  outer 
wall  of  the  cavernous  sinus. 

Nearly  all  the  intra-cranial  venous  blood  leaves  the  skull  by 
the  internal  jugular  veins,  so  that  in  an  infective  thrombosis  of 
any  of  the  cerebral  sinuses  it  may  become  necessary  to  ligature 
the  internal  jugular  vein  to  prevent  a  general  pyaemia. 

^   Bulletin  of  Johns  Hopkins  Hospital,  1912,  vol.  xxiii.  p.  321. 


Fig 


35. — Thrombosis  of  left 
cavernous  sinus. 


CHAPTEF{   III 

METHOD   OF  CASE-TAKING 

In  no  class  of  maladies  is  a  thorough  examination  of  the  patient 
of  greater  importance  than  in  cases  of  nervous  disease.  One  can- 
not urge  too  strongly  the  value  of  systematic  examination,  though 
it  matters  little  what  particular  scheme  of  case-taking  be  adopted, 
so  long  as  it  is  one  which  ensures  that  the  investigation  is  complete, 
and  that  no  point  of  importance  is  overlooked.  Sometimes,  it  is 
true,  we  may  make  a  diagnosis  at  a  glance,  as  for  example  in 
paralysis  agitans,  or  chorea.  But  more  usually  the  patient  pre- 
sents symptoms  or  signs  which  are  common  to  several  diseases, 
and  we  have  to  decide  from  which  of  these  diseases  he  is  suffering. 
The  chief  causes  of  wrong  diagnosis  are  insufficient  examination, 
inaccurate  observation,  and,  less  commonly,  false  conclusions 
from  correct  and  sufficient  facts.  But  if  we  pursue  a  good  routine 
method  of  examination,  gross  errors  of  diagnosis  can  generally 
be  avoided. 

Examination  of  a  nervous  case  should  not  be  confined  to  the 
nervous  system  alone.  All  the  systems  of  the  body  should  be 
investigated.  An  accomplished  neurologist  must  be  in  the  first 
place  a  sound  physician. 

The  value  of  negative  as  well  as  positive  facts  cannot  be 
over-estimated.  The  neurological  student  should  accustom  him- 
self from  the  outset  not  only  to  chronicle  deviations  from  the 
normal,  but  also,  if  he  finds  that  certain  other  functions  are 
normal,  to  record  the  fact  and  not  to  pass  them  over  without 
reference. 

As  in  any  other  case,  a  careful  history  should  first  be  obtained. 

It  is  comparatively  seldom  that  a  patient,  however  willing  he  may 

be,  provides    us   spontaneously  with   an   accurate   history  of  his 

case.     We  generally  have  to  guide  his  tale  by  suitable  questions, 

and  in  many  cases  we  have  to  supplement  the  patient's  account 

by  inquiring  for  corroborative  or  correcting  facts  from  the  patient's 

friends. 

55 


56  NERVOUS   DISEASES 

We  first  inquire  as  to  tlie  mode  of  onset  of  the  patient's 
symptoms,  whether  such  onset  was  sudden  or  gradual,  and,  if 
gradual,  the  exact  order  in  which  the  various  symptoms  appeared. 
In  the  family  history,  inquiry  should  be  made  as  to  the  occur- 
rence of  nervous  or  mental  disease  in  other  members  of  the  family, 
also  as  to  a  family  history  of  gout,  asthma,  tuberculosis,  cancer, 
&c.  In  certain  cases,  consanguinity  of  the  parents  should  be 
inquired  for.  In  the  account  of  the  patient's  frevious  health,  it  is 
important  to  inquire  as  to  syphilis,  kidney  disease,  gout,  rheumatic 
fever,  or  any  previous  nervous  disease,  and  a  note  should  be  made 
as  to  the  patient's  occupation  and  habits  of  life,  and  as  to  his 
temperance  in  alcohol,  tobacco,  &c.  When  inquiring  about  venereal 
disease,  if  the  patient  is  a  man,  we  should  put  our  questions  straight- 
forwardly, but  in  female  patients  considerable  delicacy  is  necessary, 
and  it  is  advisable  simply  to  inquire  for  collateral  symptoms, 
e.g.  rashes,  falling  out  of  hair,  sore  throat  and,  especially  in  married 
women,  a  succession  of  premature  or  dead  children.  In  any  case 
we  should  never  interrogate  a  male  patient  on  the  subject  of 
venereal  disease  in  the  presence  of  his  wife,   nor  vice  versa. 

Having  thus  noted  the  chief  points  in  the  history  of  the  case, 
we  proceed  to  the  examination  of  the  patient's  present  state.  The 
following  scheme  will  be  found  useful : — 

Scheme  for  Routine  Examination  of  Nervous  System. 

Higher  Cerebral  and  Mental  Functions. 

Intelligence — Attention — Memory — Emotional  state — Hallucinations  or 
delusions — Delirium — Coma — Drowsiness — Insomnia. 

Fits  or  other  Abnormal  Movements. 

Fits  —  Tremors  —  Fibrillary  movements  —  Chorea  —  Athetosis  —  Tic  — 
Myoclonus,  Myotonus,  &c.     Description  of  each. 

Speech  and  Articulation. 

Aphasia — Is  patient  riglit  or  left  handed  ? 

Cranial  Nerves. 

1.  Smell — Anosmia — Parosmia. 

2.  Visual  acuity — Fields  of  vision  :  Hemianopia,  &c. — Colour-blindness 

— Ophthalmoscopic  examination — optic  discs,  atrophy,  neuritis — 

retinal  hseraorrhages,  choroiditis,  &c. 

„  ■\  Pupils  :  Size,  shape,  reaction  to  light  (direct  and  consensual),  and 

.■  \_       to  accommodation — External  ocular  movements — Ptosis — Move- 

g'  I        ments  of  eyes  in  all  directions — Convergence — Squint — Diplopia 

'J        — Nystagmus. 
5.  Sensation — Face  :  Conjunctival,  nasal,  and  buccal  mucous  membranes 
—Taste. 
jNIotor — masseters,  temporals,  pterygoids,  &c. 


METHOD    OF    CASE-TAKING  57 

7.  Facial  muscles,  upper  and  lower — Chorda  tympaui  :  taste  in  anterior 

two-thirds  of  tongue — Nerve  to  stapedius — hyperacousis. 

8.  Hearing:   Aerial  and  Ijone  conduction — Examination  of  meatus  and 

tympanic  membrane — Tinnitus — Vertigo — Thermic  nystagmus- 
Deviation  tests. 

9.  Taste:  Posterior  third  of  tongue — Ansestliesia  of  pharynx — Difficulty 

in  swallowing. 

10.  Palate — Recurrent  laryngeal  hrancli— Laryngoscopic   examination — 

Heart,  respiration,  digestion. 

11.  Sterno-niastoid  and  Trapezius. 

12.  Tongue  (motor). 

Sensory  Functions. 

Subjective  sensations  :  Pain  : — site,  direction  of  radiation,  character, 
frequency — Headache — Vertigo — Tingling — " Pins  and  needles" 
— Formication,  &c. 

Sensibility  to  touch  —  pain  —  temperature  —  Localisation  of  the  spot 
touched — Vibration-sense  (with  tuning-fork) — Antesthesia — Par- 
sesthesia — Hypersesthesia — Tenderness  on  pressure  over  nerve- 
trunks,  muscles,  or  skin— Joint-sense — Sense  of  active  inuscular 
contraction  with  different  weights — Stereognosis. 

Motor  Functions. 

Paralysis  or  Paresis : — In  head  and  neck,  upper  limbs,  diaphragm,  inter- 
costals,  spinal  and  abdominal  muscles,  lower  limbs. 

Monoplegia — Hemiplegia — Diplegia — Paraplegia — Hemi  -  para- 
plegia— "  Crossed  paralysis,"  &c. 

Co-ordination : — Unsteadiness  of  upper  or  lower  limbs  on  voluntary  move- 
ment— Deviation  tests  after  inducing  vestibular  nystagmus — 
Finger-nose  and  heel-knee  tests — Gait. 

Muscular  Atrophy  or  Hypertrophy  :  Rigidity— Flaccidity — Hypotonia. 

Reflexes. 

Superficial. — Corneal,  palatal,  epigastric,  abdominal,  cremasteric,  plantar 
(flexion  or  extension  of  hallux) — bulbo-cavernosus — anal. 

Deep. — Jaw,  wrist,  elbow,  knee,  ankle-jerks.  Ankle-clonus — knee- 
clonus,  &c. 

Organic. — Micturition — Retention — Retention  with  overflow  incontinence 
—  Intermittent  incontinence  —  Constant  paralytic  dribbling — 
Defaecation— Control  of  sphincters — Priapism. 

Trophic  Functions. 

Muscles. — Electrical  reactions — Faradic — Galvanic — Condenser  shocks. 
Skin. — BuUiP— Herpes — Bed-sores^ — Perforating  ulcers— Glossy  skin,  &c. 
Joints  and  Bones. — Arthropathies — Spontaneous  fractures — Pes  cavus,  &c. 

Examination  of  Skull  and  Vertebral  Column. 

Abnormal  projections  or  depressions- — Tenderness,  &c.,  on  percussion — 
Radiography. 

Cerebro-spinal  Fluid. 

Naked-eye  characters  of  fluid — Microscopic  examination — Cytology — 
Bacteriology — Wassermann  reaction — Albumin,  globulin,  &c. 


58  NERVOUS    DISEASES 

Vegetative  Nervous  System. 

Cervical  sympatlietic — Dilatation  of  pupil  to  shade  and  cocaine — Cilio" 
spinal  reflex  —  Proptosis  — ■  Exophthalmos  — ■  Enoplithalmos — Re~ 
traction  of  upper  lid — Pseudo-ptosis — -Flushing  or  sweating  of 
face,  neck,  upper  extremity. 

Angio-neuroses — Raynaud's  disease — Erythromelalgia — Angio-neuiotic 
03dema — Localised  hyperidrosis  or  anidrosis — Intermittent  claudi- 
cation, &c. 

Several  points  should  be  noticed  in  the  foregoing  scheme.  We 
begin  with  the  higher  cerebral  and  mental  functions,  for  this 
reason,  that  if  a  patient  be  mentally  obtuse,  or  worse,  if  he  be 
confused  or  delirious,  then  any  statement  he  may  make  is  open  to 
doubt,  and  for  our  diagnosis  we  must  rely  mainly  (and  in  cases 
of  coma  entirely),  upon  physical  signs  and  upon  the  history 
supplied  by  the  patient's  friends. 

The  patient's  emotional  state  is  sometimes  of  diagnostic  signifi- 
cance. Not  only  are  many  hysterical  patients  unduly  emotional, 
but  a  similar  condition  is  observed  in  certain  cases  of  disseminated 
sclerosis,  where  there  is  a  tendency  to  smile  and  giggle  upon  sKght 
provocation,  whilst,  on  the  other  hand,  cases  of  aphasia  and  of 
advanced  bulbar  palsy  are  often  lachrymose. 

The  statements  of  a  patient  who  is  addicted  to  alcoholic  in- 
temperance or  to  chronic  poisoning  with  opium,  cocaine  or  other 
drug,  must  also  be  received  with  philosophic  doubt.  There  is 
a  special  variety  of  loss  of  memory,  called  Korsakow's  psychosis, 
which  occurs  chiefly  in  chronic  alcoholists,  where  the  patient, 
who  is  usually  a  woman  and  the  subject  of  peripheral  neuritis 
(most  commonly  alcoholic,  but  sometimes  due  to  other  toxic 
causes,  such  as  arsenic,  septicaemia,  &c.),  has  a  faulty  conception 
of  time  and  place  and  a  specially  deficient  memory  for  recent 
events.  Moreover  she  frequently  suffers  from  "  mythomania  "  and 
has  what  are  euphemistically  called  "  pseudo-memories,"  so  that 
"  the  truth  is  not  in  her."  This  is  one  of  the  toxic  varieties  of 
insanity,  and  is  commoner  in  women  than  in  men.  Male  alcoholists 
seldom  show  Korsakow's  psychosis,  but,  if  the  alcohol  be  suddenly 
withdrawn  {e.g.  during  an  acute  illness  or  accident),  they  tend  to 
sufEer  from  the  more  violent  and  dramatic  "  delirium  tremens," 
with  the  tremors,  acute  distress,  and  hallucinations  of  rats,  beetles, 
devils,  &c.  (zoopsia),  so  familiar  to  the  lay  writer. 
[^  i  Passing  from  the  patient's  mental  condition,  we  should  carefully 
observe    and  describe   any    fits,    tremors,    or  other    spontaneous 


METHOD    OF    CASE-TAKING  59 

abnormal  movements  that  may  be  present.  Disorders  of  speech 
and  articulation  should  next  be  studied,  and  the  cranial  nerves 
examined  in  due  order. 

It  will  be  observed  that,  in  our  scheme  of  case-taking,  sensory 
functions  are  investigated  before  motor.  As  a  matter  of  experi- 
ence, this  order  of  examination  is  found  to  be  of  considerable 
practical  advantage.  The  discovery  of  an  area  of  anaesthesia 
often  puts  us  rapidly  on  the  track  of  a  correct  diagnosis  and 
enables  us  to  select  with  greater  ease  the  salient  points  in  the 
motor  and  other  phenomena. 

Certain  accessory  methods  of  examination,  such  as  the  testing 
of  electrical  reactions  and  lumbar  puncture,  are  required  only 
in  special  circumstances,  where  they  may  throw  a  flood  of  light  on 
an  otherwise  obscure  case.  Inspection,  palpation,  and  percussion 
of  the  skull  are  of  considerable  value  in  some  cases  of  tumour  of 
the  brain,  especially  in  cases  of  cerebellar  growths.  Sometimes  it 
is  advisable  to  have  the  scalp  shaved,  in  order  to  detect  abnor- 
malities in  the  shape  of  the  cranium. 

Having  collected  our  facts,  comprising  the  history  and  the 
present  state  of  the  patient,  we  are  now  in  a  position  to  make  our 
diagnosis.  And  in  the  process  of  diagnosis  we  have,  first  of  all, 
to  ask  ourselves — Is  the  disease  an  organic  one,  due  to  a  gross 
irritative  or  destructive  lesion  in  the  nervous  system,  for 
example  cerebral  haemorrhage,  alcohohc  neuritis  or  tuberculous 
meningitis  ?  Or  is  it  one  of  the  so-called  "  functional "  diseases, 
that  is  to  say,  without  known  morbid  anatomy,  for  example 
hysteria,  migraine,  neurasthenia  ? 

The  boundary-line  between  functional  and  organic  diseases  is  not 
so  definite  as  might  at  first  sight  be  supposed.  At  the  present  day, 
many  diseases  are  classified  as  functional,  for  no  better  reason  than 
that  in  them  no  constant  anatomical  changes  have  yet  been  recognised. 
In  such  diseases  as  epilepsy,  paralysis  agitans,  exophthalmic  goitre, 
and  Raynaud's  disease,  there  can  be  little  doubt  that  profound  mole- 
cular changes  exist — in  the  two  former  instances  in  the  central  nervous 
system,  in  the  two  latter  in  the  vegetative  system — but  these  changes 
have  not  yet  been  recognised.  Other  diseases  again,  due  to  poisoning 
by  microbes  or  their  toxins,  or  by  other  poisons — e.g.  chorea,  hydro- 
phobia, tetanus,  certain  varieties  of  epileptiform  fits,  &c. — are  un- 
doubtedly the  result  of  pathological  changes  affecting  various  groups 
of  nerve  elements.  And  yet,  because  at  present  these  changes  are 
not  visible  histologically,  they  have  been  classed  as  "  functional." 
Even  hysteria  itself,  the  prototype  of  functional  diseases,  has  some 


60  NERVOUS    DISEASES 

profound  underlying  bio-chemical  change.  The  term  "functional," 
then,  is  a  confession  of  our  etiological  ignorance,  and  is  by  no  means 
synonymous  with  "  curable,"  as  the  steady  and  progressive  advance 
of  such  a  disease  as  paralysis  agitans  readily  shows. 

If  the  evidence  points  to  an  organic  lesion,  we  have  then  to 
ask  ourselves  two  further  questions :  (1)  Where  is  the  lesion  ? 
(2)  What  is  its  pathological  nature  ?  The  answer  to  the  first 
question,  which  constitutes  the  anatomical  diagnosis,  is  derived 
mainly  from  a  study  of  the  distribution  and  grouping  of  the  signs 
and  symptoms.  The  answer  to  the  second,  constituting  the  'patho- 
logical diagnosis,  is  attained  mainly  by  a  study  of  the  history  of 
the  mode  of  onset  and  the  rate  at  which  the  lesion  develops. 

In  making  an  anatomical  diagnosis  we  should  always  endeavour 
to  think  of  a  single  lesion  which  will  account  for  all  the  symptoms. 
Thus,  for  example,  if  a  patient  comes  to  us  with  hemiplegia  of  the 
left  arm  and  leg,  of  the  "  upper  motor  neurone  "  type  (see  p.  35), 
and  at  the  same  time  a  right- sided  facial  palsy  of  the  "  lower 
motor  neurone "  type,  instead  of  diagnosing  two  lesions,  one 
in  the  right  side  of  the  brain  causing  left  hemiplegia  and  another 
in  the  right  facial  nerve  causing  right  facial  palsy,  we  prefer 
to  diagnose  a  single  lesion  in  the  right  side  of  the  pons,  impli- 
cating simultaneously  the  right  facial  nerve  and  the  pyramidal 
tract  (see  Fig.  6). 

As  an  example  of  pathological  diagnosis,  suppose  we  have  a 
patient  with  spastic  paraplegia  of  both  lower  limbs  and  anaesthesia 
up  to  the  level  of  the  umbilicus,  the  anatomical  position  of  the 
lesion  is  comparatively  easy  to  fix,  namely  in  the  lower  thoracic 
region  of  the  cord,  implicating  both  sensory  and  motor  tracts.  If  the 
symptoms  appeared  suddenly,  we  think  of  a  vascular  lesion  such 
as  haemorrhage  or  thrombosis ;  if  they  developed  within  a  day  or 
two,  some  inflammatory  condition  such  as  myehtis  is  probable  ; 
whilst  if  they  only  appeared  very  slowly,  taking  many  months 
to  reach  their  present  intensity,  we  have  to  think  of  a  slowly  pro- 
gressive lesion,  such  as  a  tumour. 

We  must  never  diagnose  hysteria  or  neurasthenia  until  we 
have  excluded  gross  organic  disease.  And,  finally,  we  should  re- 
member that  the  presence  of  certain  hysterical  or  neurasthenic  symp- 
toms does  not  exclude  a  co-existent  organic  lesion,  nor  vice  versa. 
Functional  and  organic  disease  may  be  combined  in  the  same 
patient,  and  this  combination  increases  the  difficulty  of  diagnosis. 


METHOD    OF    CASE-TAKING 


Gl 


In  such  cases  the  functional  element  is  usually  more  extensive 
in  distribution  than  the  underlying  organic  part,  and,  as  it  were, 
submerges  it.  Unless  care  be  exercised  in  the  examination,  the 
organic  factor  may  either  be  overlooked  and  the  whole  case  wrongly 
regarded  as  functional,  or,  on  the  other  hand,  the  organic  paralysis 
may  appear  more  serious  than  it  really  is.  The  following  is  an  illus- 
trative example  of  combined  functional  and  organic  disease  : — 

A  gunner,  aged  twenty-seven,  was  hit  by  a  shrapnel  bullet  at 
Grallipoli.  The  entry-wound  was  through  the  middle  of  the  left  upper 
arm,  behind  the  musculo-spiraljgroove  ;  the  exit-wound  was  an  inch 
higher  up,  through  the  middle  of  the  biceps.  The  bullet-track  thus 
crossed  the  musculo- 
spiral  nerve.  The 
patient's  upper  limb 
at  once  dropped 
powerless  to  his  side  ; 
he  himself  felt  as  if  it 
had  been  blown  off. 
He  had  no  pain  at  the 
time  of  injury,  nor 
afterwards. 

When  examined, 
eight  days  after  the 
injury,  there  was 
complete  anaesthesia 
of  the  left  upper  limb 
to  all  forms  of  cutan- 
eous stimulation, from 
the  level  of  the  acro- 
mion downwards  (see 
Fig.  35a).  Joint-sense 
was  absent  at  the  fingers  and  wrist,  normal  at  the  elbow  and  shoulder. 
Vibration-sense  was  lost  in  the  hand,  forearm,  and  upper  arm,  normal 
at  the  clavicle  and  scapula. 

The  only  voluntary  movement  that  could  be  performed  in  the  left 
upper  limb  was  feeble  flexion  of  the  fingers.  The  thumb,  wrist,  and 
forearm  were  completely  paralysed.  The  biceps  and  triceps  could 
be  felt  feebly  to  contract,  but  not  enough  to  move  the  elbow.  He 
could  feebly  abduct  and  adduct  the  shoulder. 

To  faradism  there  was  loss  of  reaction  in  the  supinator  longus  and 
in  the  extensors  of  the  wrist,  fingers,  and  thumb.  All  the  other  muscles 
of  the  upper  limb  reacted  briskly. 

Fig.  35a  shows  the  patient  during  an  attempt  to  flex  both  elbows 
and  to  dorsiflex  both  wrists.  On  the  left  side  he  fails  to  do  so.  There 
is  wrist  drop,  and  the  elbow  is  being  passively  dorsiflexed  by  the  nurse. 
The  entry-wound  behind  the  musculo -spiral  nerve  is  shown,  also  the 
upper  limit  of  the  cutaneous  anaesthesia. 


Fig.  35a. — Paralysis  of  left  musculo-spiral  ner%'-e,  to 
which  is  superadded  a  hysterical  monoplegia  of  the 
whole  upper  limb. 


CHAPTER   IV 

COMA 

We  are  not  infrequently  called  to  see  a  patient  who  is  found  to  be 
unconscious.  In  such  cases  it  is  of  great  importance  to  make  a 
correct  diagnosis  as  to  the  probable  cause.  There  are  different 
degrees  of  unconsciousness.  For  example,  there  are  conditions 
in  which  the  patient  can  be  roused  from  his  unconsciousness 
by  shaking,  shouting,  or  other  stimuli,  as  in  the  case  of  ordinary 
sleep.  When  this  degree  of  unconsciousness  occurs  in  pathological 
conditions,  as  in  a  patient  stupefied  by  various  poisons  (whether 
produced  within  the  body  or  introduced  from  without),  or  from 
mechanical  compression  of  the  brain,  for  example  by  haemorrhage, 
we  call  the  condition  stupor. 

Cerebral  Concussion,  resulting  from  head-injury,  is  a  condition 
in  which  the  patient  is  pale  and  collapsed,  with  a  blood-pressure 
lowered  to  80  or  70  mm.  of  Hg  or  even  less.  He  may  be  stuporose 
or  even  comatose.  In  a  slight  case  there  is  merely  temporary 
unconsciousness  or  giddiness,  with  pallor  and  a  little  mental  con- 
fusion, often  followed  by  headache.  In  more  severe  cases  there 
is  an  initial  stage  of  collapse  with  unconsciousness  lasting  for  hours 
or  even  for  days.  But  in  most  cases  the  patient  can  be  roused  by 
strong  stimuli.  His  face  is  pale,  his  pupils  dilated,  his  breathing  is 
slow,  shallow,  and  irregular  ;  his  pulse  is  weak  and  his  temperature 
subnormal.  He  Ues  with  flaccid  limbs,  Uke  a  drunken  man. 
Trendelenburg  has  aptly  named  this  condition  "  traumatic 
narcosis."  Then  comes  the  stage  of  reaction,  often  ushered  in  by 
vomiting,  sometimes  even  by  an  epileptiform  convulsion.  Con- 
sciousness begins  to  return  ;  the  temperature  rises  and  may  mount 
to  100°  F.  or  higher,  the  pulse  is  now  full  and  bounding,  and  the 
respirations  become  deeper.  There  is  usually  headache.  Such  a 
patient  generally  has  a  "  retrograde  amnesia,"  i.e.  he  has  no 
recollection  of  the  incidents  which  occurred  within  the  last  few 
hours  immediately  prior  to  his  accident.  As  a  rule,  although  the 
memory  of  these  incidents  returns  later,  the  remembrance  of  the 
accident  itself  is  permanently  lost. 

62 


COMA  63 

Coma  is  that  degree  of  unconsciousness  which  is  so  deep  that 
we  are  unable,  by  any  ordinary  stimulus,  to  rouse  the  patient. 
A  deeply  comatose  patient  does  not  swallow  fluids  placed  in  his 
mouth,  his  conjunctival  reflexes  are  absent  and  his  pupils  in- 
sensitive to  light,  as  in  deep  chloroform  anaesthesia. 

How  are  we  to  proceed  when  called  to  see  a  patient  whom 
we  find  comatose  ?  Firstly,  we  inquire  into  the  history,  as  to  the 
patient's  previous  health,  whether  the  coma  was  sudden  or  gradual 
in  onset  and  whether  it  was  preceded  by  other  symptoms,  such  as 
convulsions  or  headache.  We  then  examine  the  patient,  feel  the 
head  for  signs  of  injury,  smell  the  breath,  examine  the  pupils, 
noting  their  size,  equality  or  inequality,  and  their  reaction  to 
light ;  we  listen  to  the  heart  and  note  the  character  and  frequency 
of  the  pulse  and  respirations.  We  note  the  radial  systolic  blood- 
pressure  and,  if  possible,  measure  it  by  means  of  a  sphygmo- 
manometer. We  observe  whether  the  face  is  symmetrical  or 
not,  and  whether  there  is  conjugate  deviation  of  the  head  and 
eyes  in  any  direction.  The  optic  discs  in  all  cases  should 
be  examined.  We  lift  the  limbs  in  turn  and  let  them  fall, 
observing  whether  there  is  any  difference  between  the  flaccidity 
of  the  two  sides.  We  also  test  the  knee-jerks  and  examine  the 
abdominal  and  plantar  reflexes  on  both  sides.  Then  we  pass  a 
catheter,  draw  off  the  urine,  note  its  specific  gravity  and  test 
it  for  albumin  and  for  sugar.  Finally  we  note  the  temperature 
in  both  axillae,  and  in  certain  cases  we  perform  lumbar  puncture 
and  examine  the  cerebro- spinal  fluid. 

The  first  question  is  whether  the  coma  is  due  to  a  general 
toxaemia,  such  as  poisoning  by  alcohol  or  opium,  uraemia,  dia- 
betes, &c.,  or  whether  it  is  the  result  of  some  gross  intra-cranial 
lesion,  such  as  haemorrhage,  meningitis,  abscess,  tumour,  &c. 

As  a  general  maxim  we  may  state  that,  if  coma  be  toxaemic  in 
origin,  practically  all  the  signs  and  symptoms  will  be  bilaterally 
symmetrical.  On  the  contrary,  most  cases  of  gross  intra-cranial 
disease  being  unilateral,  or  at  least  asymmetrical,  there  will  there- 
fore be  a  corresponding  preponderance  of  symptoms  on  one  side 
of  the  body,  so  that,  in  addition  to  coma,  we  have  a  number  of 
unilateral  signs.     Let  us  consider  these  unilateral  cases  first. 

The  commonest  case  is  that  of  spontaneous  cerebral  haemorrhage. 
Here  the  onset  of  unconsciousness  is  generally  sudden ;  the 
patient's  face  is  flushed,  or  cyanosed,  his  skin  sweats  profusely, 


64  NERVOUS    DISEASES 

he  breathes  stertorously,  his  blood-pressure  is  high,  and  his  pulse 
is  slow,  full  and  bounding.  AH  his  limbs  are  flaccid,  but  on 
comparing  the  two  sides,  we  find  that  the  flaccidity  is  more 
absolute  on  the  hemiplegic  side.  For  example,  the  elbow  of  the 
affected  side  can  be  passively  flexed  to  a  greater  degree  than 
that  of  the  healthy  side.  The  arm  and  leg  on  the  paralysed 
side  also  fall  more  "  dead "  than  do  those  of  the  sound  side 
when  hfted  up  in  turn  and  allowed  to  drop.  The  paralysed 
leg  lies  extended,  whereas  the  healthy  one  tends  to  be  semi- 
flexed. The  head  and  eyes  are  often  turned  to  one  side, 
generally  away  from  the  paralysed  limbs,  unless  the  haemorrhage 
be  cortical  or  intra-ventricular,  in  which  cases  the  deviation 
may  be  toward  the  paralysed  limbs,  and  is  associated  with 
other  irritative  phenomena,  e.g.  spasticity  instead  of  flac- 
cidity. The  face  is  asymmetrical,  especiaUy  its  lower  part,  the 
paralysed  cheek  flaps  loosely  during  respiration  and  the  mouth 
is  distorted  like  a  mark  of  exclamation  laid  on  its  side  (!— ),  as  if 
the  patient  were  "  puffing  his  pipe  "  at  the  paralysed  angle  of  the 
mouth.  The  pupils  are  generally  dilated  and  sometimes  unequal, 
the  larger  pupil  being  on  the  side  of  the  brain  lesion.  In  pontine 
haemorrhage,  however,  the  pupils  are  often  contracted  to  pin- 
points. At  the  onset  of  an  ordinary  apoplexy,  whilst  we  get  little 
help  from  the  deep  reflexes,  which  may  or  may  not  be  diminished 
or  lost  on  the  affected  side,  there  is,  from  the  very  outset, 
an  extensor  plantar  reflex  in  the  toes  of  the  hemiplegic  foot, 
and  all  the  other  superficial  reflexes  on  that  side  are  diminished 
or  absent.  The  skin  of  the  abdomen  can  be  pinched  or  pricked 
on  the  paralysed  side  without  eHciting  an  abdominal  reflex — 
(Rosenbach's  sign).  The  corneal  reflex  is  abolished  on  the  hemi- 
plegic side  instead  of  on  both  sides  as  in  toxic  coma.  The 
temperature  on  the  paralysed  side  is  usually  higher  than  on  the 
other,  although  the  general  temperature  of  the  whole  body  falls 
at  first.  If  the  coma  has  lasted  several  hours,  the  bladder  becomes 
distended  and  may  develop  an  overflow  incontinence.  Afterwards, 
the  temperature  rises  above  normal,  and  in  bad  cases  may  go  on 
to  hyper-pyrexia. 

Most  cases  of  spontaneous  cerebral  haemorrhage  occur  in  patients 
past  middle-age,  in  whom  the  arteries  are  no  longer  elastic  and 
healthy,  and  there  is  often  a  history  of  kidney  disease,  with  its 
resultant  cardiac  hjrpertrophy  and  high-tension  pulse,  conditions 


COMA  65 

particularly  liable  to  result  in  the  bursting  of  a  cerebral  artery. 
The  actual  attack  of  haemorrhage  not  uncommonly  occurs  during 
some  slight  physical  exertion  or  mental  excitement,  as  in  public 
speakers,  such  as  clergymen,  politicians,  or  after-dinner  orators, 
or  in  old  people  with  brittle  arteries,  during  straining  at  stool.  In 
most  cases  of  intra-dural  cerebral  haemorrhage  from  whatever 
cause,  the  cerebro-spinal  fluid  is  tinged  with  blood  in  greater  or 
smaller  amount. 

But,  in  rare  cases,  cerebral  haemorrhage  may  also  occur  in  young 
people  having  healthy  vessels,  as,  for  example,  in  a  child  during 
violent  convulsions  or  during  a  paroxysm  of  whooping-cough,  when 
the  haemorrhage  is  commonly  venous  in  origin  (due  to  passive  con- 
gestion with  rupture  of  the  cortical  veins),  and  subdural  in  situa- 
tion, or  it  may  occur  in  any  of  the  so-called  "  bleeding  diseases  " — 
purpura,  haemophilia,  leukaemia,  &c.,  especially  after  some  trivial 
injury. 

Cerebral  haemorrhage  often  occurs  in  cases  of  general  paralysis 
of  the  insane,  and  in  fact  may  be  the  first  symptom  calling 
attention  to  the  disease.  The  symptoms  are  those  already 
described,  but  there  is  usually  a  history  of  previous  mental 
failure,  grandiose  ideas,  loss  of  memory,  attacks  of  emotional 
excitement,  and  slight  indistinctness  of  articulation.  In  the 
absence  of  such  history,  we  may  be  unable  at  the  time  to  diagnose 
anything  more  than  the  fact  of  a  cerebral  haemorrhage.  But 
afterwards,  when  the  patient  recovers  from  his  apoplexy — and  the 
general  paralytic  recovers  much  more  rapidly  than  the  non-insane 
patient — we  can  generally  recognise  the  characteristic  evidences 
of  the  disease,  both  psychical  and  physical 

Coma  may  also  be  due  to  traumatic  cerebral  "compression," 
where  there  is  a  haematoma  on  the  surface  of  the  brain,  either 
intra-  or  extra-dural.  The  signs  are  practically  the  same  as  in 
spontaneous  apoplexy  but  the  onset  is  different,  for  there  is  a 
history  of  a  head  injury.  The  symptoms  develop  gradually, 
especially  if  the  haemorrhage  be  extra-dural,  beginning  with  local 
paralysis  and  perhaps  localised  convulsions.  The  paralysis  gradually 
increases,  the  patient  becomes  drowsy,  stupid,  and  finally  comatose, 
the  blood-pressure  meanwhile  rising  to  an  excessive  degree.  There 
may  be,  before  the  onset  of  coma,  a  "  lucid  interval "  of  several 
hours  or  even  a  whole  day,  during  which  the  patient,  who  was 
perhaps  only  stunned  by  the  original  blow,  recovers  consciousness 

E 


66  NERVOUS    DISEASES 

and  is  apparently  normal.  A  lucid  interval  of  this  duration, 
when  followed  by  the  above  symptoms,  generally  indicates  that 
the  haemorrhage  is  extra-dural.  In  intra-cranial  haemorrhage 
oedema  of  the  retina  often  supervenes  within  a  few  hours. ^  The 
oedema  is  more  intense  in  the  eye  on  the  same  side  as  the  focal 
compression,  and  this  fact  may  be  of  diagnostic  value  in  obscure 
cases  of  coma  following  head-injuries.  This  retinal  oedema  rapidly 
subsides  if  the  intra-cranial  tension  be  relieved  by  operation.  It 
is  uncommon  for  symptoms  of  compression  to  come  on  immedi- 
ately after  the  head  injury,  and  when  they  do  so,  they  suggest  a 
depressed  fracture  pressing  directly  upon  the  brain.  This  can 
generally  be  detected  by  examination  of  the  cranium. 

Another  important  form  of  cerebral  haemorrhage  which  pro- 
duces cerebral  compression  is  chronic  subdural  haemorrhage  or 
"  compression  tardive,"  in  which  a  collection  of  blood,  often  very 
large,  gradually  accumulates  between  the  dura  mater  and  the 
cerebral  hemisphere.  This  blood  is  enclosed  within  a  distinct 
membrane,  derived  from  the  coagulated  blood  itself.  Its  longest 
diameter,  which  may  measure  four  to  six  inches,  is  usually  antero- 
posterior, most  commonly  in  the  fronto -parietal  region.  The  con- 
dition is  sometimes  bilateral.  The  bleeding  is  venous  in  origin, 
and  is  due  to  rupture  of  the  short  cerebral  veins  which  enter  the 
superior  longitudinal  sinus  almost  at  right  angles.  These  veins  are 
firmly  fixed  at  one  end  in  the  rigid  dura,  whilst  they  are  attached 
at  their  cerebral  end  to  the  relatively  movable  brain.  Chronic 
subdural  haemorrhage  is  the  result  of  a  trauma,  but  the  injury  is 
generally  comparatively  trivial,  so  much  so,  that  unless  inquired 
for,  it  may  be  entirely  overlooked.  A  sharp  blow,  especially  on 
the  front  or  back  of  the  head,  may,  without  any  fracture  of  the 
cranium,  or  even  without  a  scalp -wound,  suddenly  dislocate  the 
hemispheres  and  rupture  the  veins  on  one  or  both  sides.  The 
resulting  haemorrhage  is  a  slow  or  intermittent  venous  oozing. 
After  the  injury  there  is  usually  a  long  interval,  of  several  days  at 
least,  before  the  haemorrhage  is  large  enough  to  cause  symptoms  of 
intra-cranial  pressure.  Then  headache  appears,  severe  and  per- 
sistent, sometimes  over  the  seat  of  the  haemorrhage.  This  headache 
lasts  a  week  or  two  and  is  gradually  followed  by  slight  mental 
changes,  such  as  absent-mindedness,  sleepiness,  forgetfulness,  &c. 
This  "  prodromal  period  "  generally  lasts  about  six  weeks.     Then, 

'   Gushing,  New  York  Medical  Journal,  Janiif^ry  19,  1907. 


COMA  67 

rather  suddenly,  the  symptoms  become  much  worse  and  the 
drowsiness  quickly  deepens  to  coma.  This  may  be  ushered  in  by 
violent  headache  and  vomiting.  The  coma  is  of  a  remarkable 
type,  undergoing  curious  spontaneous  variations,  so  that  the 
patient  passes  from  consciousness  to  unconsciousness  and  vice 
versa.  There  is  no  other  clinical  condition  in  which  this  feature  is 
so  striking.  The  patient  in  the  intervals  appears  mentally  dull, 
but  not  confused.  Responses  to  simple  questions  are  made  very 
slowly,  but  quite  intelligently,  so  far  as  they  go.  The  physical 
signs  of  focal  cerebral  lesion  are  variable,  slight,  and  elusive. 
Pressure  by  the  effused  blood  on  the  motor  cortex  may  produce 
monoparesis  or  hemiparesis  of  leg  and  arm,  the  face  generally 
being  unaffected.  An  extensor  plantar  reflex  and  diminution  or 
loss  of  the  abdominal  reflex  are  perhaps  the  most  valuable  uni- 
lateral signs.  The  extensor  response  may,  however,  be  bilateral, 
even  with  a  unilateral  lesion,  probably  from  dislocation  of  the 
opposite  motor  cortex  against  the  cranium.  Pressure  on  the  mid- 
brain may  produce  ocular  or  pupillary  changes.  Optic  neuritis 
may  develop.  In  unilateral  lesions  it  is  usually  most  marked  on 
the  side  of  the  lesion.  In  bilateral  lesions,  it  tends  to  be  most 
intense  on  the  side  of  the  greater  lesion.  Respiration  is  often 
peculiar — like  that  of  a  healthy  person  sleeping  soundly — i.e.  a 
little  exaggerated  in  amplitude  and  with  expiration  slightly 
emphasized.  This  can  be  observed  when  the  patient  is  apparently 
awake.  The  haemorrhage  is  often  bilateral,  thereby  confusing  the 
clinical  picture.  Correct  diagnosis  is  of  great  importance,  since  the 
condition  is  amenable  to  surgical  treatment,  and  if  the  blood-cyst 
be  evacuated  and  drained,  complete  recovery  may  occur.  Spon- 
taneous recovery  is  unlikely.  Chronic  subdural  hsemorrhage  is 
probably  identical  with  the  condition  known  as  pachymeningitis 
hcemorrhagica  interna,  which  is  associated  with  general  paralysis, 
with  chronic  alcoholism,  and  with  senile  dementia.  The  condition 
has  usually  been  assumed  to  be  a  spontaneous  subdural  venous 
haemorrhage,  but,  as  Trotter  points  out,  alcoholic  and  insane  patients 
are  exactly  those  who  are  particularly  exposed  to  the  moderate 
kind  of  injury  which  is  especially  prone  to  produce  chronic  sub- 
dural haemorrhage,  and  the  patient  is  not  likely  to  remember  or 
make  much  of  the  accident.  ^ 

Pontine  Hsemorrhage  is  generally  near  the  middle  line,  and 

1  Trotter,  Brit,  Journal  of  Surgery,  vol.  ii,,  1914,  p.  271. 


68  NERVOUS    DISEASES 

therefore  tends  to  produce  bilateral  symptoms.  Pontine  cases 
generally  (but  not  always)  have  strongly  contracted  pupils  owing 
to  irritation  of  the  third  nerve  nuclei.  There  is  often  hyper- 
pyrexia and  most  cases  are  fatal. 

Thrombosis  of  the  Cerebral  Sinuses  is  a  rarer  cause  of  coma. 
Here  the  diagnosis  rests  chiefly  on  the  history.  Cases  secondary 
to  suppurative  conditions  of  the  middle  ear  or  frontal  sinuses  will 
have  a  corresponding  history  and  the  other  signs  of  intra-cranial 
venous  obstruction.  Primary  thrombosis  of  a  sinus,  occurring 
without  infection,  as  in  marasmus,  profound  anaemia,  &c.,  is  ex- 
cessively difficult  to  recognise.  Thromhosis  of  cerebral  arteries, 
producing  cerebral  softening,  often  causes  hemiplegia,  but  its  onset 
is  slower  than  is  that  of  hsemorrhage ;  it  more  often  comes  on 
during  ordinary  sleep  and  is  rarely  associated  with  coma.  In 
young  patients  it  is  generally  syphihtic  in  origin. 

In  old  people  the  commonest  variety  of  non-fatal  hemiplegia  is 
the  so-called  lacunar  hemiplegia,  due  to  the  occurrence  of  small 
lacunar  foci  of  peri-arterial  disintegration.  The  onset  is  sudden, 
but  is  rarely  associated  with  unconsciousness.  On  the  contrary, 
the  old  man,  as  it  were,  supervises  his  hemiplegic  attack  :  he 
suddenly  notices  paresis  and  flaccidity  of  the  limbs  on  one  side, 
usually  more  marked  in  the  leg  than  the  arm.  This  hemiparesis 
clears  up  in  a  few  hours  or  days  without  leaving  behind  it  con- 
tracture in  the  paresed  limbs.  Such  attacks  tend  to  recur,  affecting 
one  or  both  sides  of  the  brain,  and  often  producing  a  curious  short- 
stepped  gait  ("  marche  a  petits  pas  "),  until  some  day  a  terminal  and 
fatal  hsemorrhage  occurs  in  and  around  one  of  the  lacunae,  pro- 
ducing coma  and  the  other  classical  signs  of  cerebral  hsemorrhage. 

Amongst  the  other  gross  intra-cranial  diseases  producing  coma, 
is  cerebral  meningitis.  Here  again  our  diagnosis  depends  on 
the  history.  Most  frequently  the  patient  is  a  child.  Instead  of 
a  history  of  sudden  coma  or  of  head  injury  we  learn  that  there  have 
been,  for  some  days,  headache,  vomiting,  photophobia  and  head- 
retraction,  and  often  the  characteristic  "  hydrocephahc  cry."  The 
child  gradually  becomes  drowsy,  apathetic,  and  finally  comatose. 
Rigidity  of  the  neck  muscles  and  head-retraction  persist  during 
the  coma  (Fig.  36).  Kernig's  sign  and  Brudzinski's  "  neck  "  and 
"  leg  "  signs  are  often  of  value.  Kernig's  sign  consists  in  a  i:eflex 
contraction  of  the  hamstring  muscles  and  a  wince  of  pain  when  an 
attempt  is  made  to  put  the  sacral  nerve-roots  on  the  stretch  by 


COMA  69 

flexing  the  hip  to  a  right  angle  and  at  the  same  time  extending 
the  knee.  Brudzinski's  neck-svjn,  which  h  even  more  frequently 
present  than  Kernig's  sign,  is  eUcited  by  first  flexing  the  arms  and 
legs  on  the  trunk  to  their  full  extent  and  then  passively  flexing  the 
head  on  the  chest.  The  patient  at  once  cries  out.  Brudzinski's 
leg-sign  is  elicited  by  passively  flexing  one  lower  limb  on  the  abdomen 
to  its  full  extent,  when  the  other  leg  is  at  once  drawn  up  by  the 
patient  to  a  similar  position.  If  the  meningitis  be  chiefly  on  the 
convexity  of  the  brain,  there  are  commonly  convulsions  preceding 
or  accompanying  the  coma.  On  the  other  hand,  if  the  meningitis 
be  mainly  basal,  there  are  cranial  nerve  paralyses,  especially  of  the 
ocular  muscles.     Examination  of  the  cerebro-spinal  fluid  obtained 


Fig.  36. — Case  of  posterior  basic  meningitis,  showing  head-retraction 
and  posture  of  limbs. 

by  lumbar  puncture  gives  conclusive  evidence  in  cases  of  suspected 
meningitis.  The  diagnosis  between  meningitis  and  cerebral  abscess, 
especially  in  cases  of  suppurative  otitis,  is  sometimes  difficult. 
Amongst  the  important  diagnostic  points  the  state  of  the  pulse  is 
of  great  value.  In  meningitis  the  pulse  tends  to  be  small,  rapid, 
and  irregular  :  in  brain-abscess  it  is  regular  and  full.  In  menin- 
gitis the  temperature  is  usually  raised  :  in  brain-abscess  it  is  often 
subnormal.  Optic  neuritis,  if  present,  will  indicate  that  the  coma 
is  not  due  to  mere  haemorrhage,  but  that  there  is  increased  intra- 
cranial pressure,  either  due  to  meningitis,  cerebral  abscess,  or 
possibly,  if  the  history  be  a  matter  of  weeks  or  months,  to  intra- 
cranial growths,  syphihtic,  tuberculous,  or  neoplastic. 

Let  us  now  pass  to  the  other  class  of  cases  of  coma,  due  not 
to  a  gross  intra-cranial  lesion,  but  to  some  general  toxic  condition 


70  NERVOUS    DISEASES 

of  the  higher  cerebral  centres.  In  this  group  the  important 
point  to  notice  is  the  absence  of  unilateral  signs. 

In  the  coma  of  opium  poisoning  there  may  be  a  history  of 
laudanum  swallowed  or  morphine  injected  hypodermically.  An 
empty  laudanum-bottle  or  a  hypodermic-syringe  may  be  found 
by  the  patient's  side  when  he  is  discovered.  If  laudanum  has 
been  taken  by  the  mouth,  ita  odour  may  be  detected  in  the 
breath.  A  chemical  analysis  of  the  stomach-contents  obtained 
by  the  stomach-tube,  will  also  help  in  the  diagnosis.  In  the 
comatose  patient  we  notice  the  excessive  slowness  of  respiration, 
the  slow  and  feeble  pulse,  the  cold  clammy  skin,  and,  most  striking 
of  all,  the  pupils  contracted  to  pin-points.  These  symptoms  might 
be  confused  with  those  of  pontine  haemorrhage.  But  there  is  not 
the  pyrexia  of  a  pontine  apoplexy,  and  the  coma  of  opium  is  not 
so  deep  as  that  of  haemorrhage.  It  used  to  be  taught  that  in  opium- 
poisoning  the  plantar  reflexes  are  of  the  normal  flexor  type,  but  I 
have  seen  a  case  in  which  a  young  man,  after  a  toxic  hypodermic 
dose  of  morphine,  became  comatose  with  absent  knee-jerks  and 
ankle- jerks,  and  with  extensor  plantar  responses.  Fortunately  he 
recovered,  and  a  few  hours  later  the  deep  reflexes  had  reappeared 
and  the  plantar  reflexes  were  again  flexor  in  type. 

The  coma  of  acute  alcoholic  poisoning  is  not  so  deep  as  that 
of  apoplexy,  for  the  patient  can  generally  be  roused,  temporarily 
at  least,  by  energetic  stimulation.  The  typical  stertor  of  apoplexy 
is  not  present,  the  pupils  are  dilated  and  react  to  light,  and  the 
corneal  reflexes  are  preserved.  The  temperature  is  subnormal, 
the  breath  and  stomach- contents  smeU  of  alcohol,  and  if  we  mix 
a  specimen  of  the  urine  with  potassium-bichromate  solution  and 
then  allow  strong  sulphuric  acid  to  flow  to  the  bottom  of  the  test- 
tube,  a  green  colour  appears  if  alcohol  be  present  in  the  urine. 

We  must  be  careful,  however,  not  to  diagnose  alcoholic  poison- 
ing simply  because  the  patient's  breath  smells  of  alcohol.  In  the 
first  place,  a  patient  with  cerebral  haemorrhage  may  have  had 
alcohol  given  him,  just  at  the  onset  of  his  symptoms.  Or  secondly, 
a  patient  who  has  been  drinking  alcohol  may  have  an  attack  of 
apoplexy,  or  he  may  fall  and  sustain  a  head  injury  causing  com- 
pression. Therefore  every  patient  with  apparent  alcohoHc  coma 
should  be  carefully  watched  for  about  twenty-four  hours,  in  case 
unilateral  paralysis,  an  extensor  plantar  reflex,  or  inequality  of  the 
pupils  should  supervene. 


COMA  71 

Post-epileptic  Coma  may  be  mistaken  for  apoplexy,  if  we  do 
not  happen  to  know  that  the  patient  is  epileptic.  But  generally 
we  have  the  history  of  preceding  fits,  and  in  a  chronic  epileptic 
there  may  be  old  scars  about  the  scalp,  tongue,  or  face,  the  result  of 
injuries  during  previous  fits.  There  is  no  preponderance  of  uni- 
lateral symptoms  after  a  general  epileptic  fit,  nor  is  there  inequality 
of  the  pupils.  The  tongue  may  have  been  bitten  during  the  fit  and 
may  be  still  bleeding  during  the  stage  of  coma.  Within  an  hour  or 
less,  the  epileptic  recovers  consciousness  without  paralytic  sequelae. 
If,  however,  some  transient  localised  motor  weakness  follows,  this 
points  rather  to  a  Jacksonian  fit  due  to  a  focal  lesion. 

In  the  Stokes-Adams  syndrome  we  have  profound  coma  and 
stertorous  breathing,  with  or  without  epileptiform  convulsions. 
The  condition  is  readily  diagnosed  by  recognition  of  the  extremely 
slow  pulse-rate.  Acceleration  of  the  pulse  precedes  recovery  from 
the  coma. 

Uraemic  Coma  is  not  uncommon,  occurring  as  it  does  in 
patients  who  are  the  subjects  of  nephritis,  acute  or  chronic. 
The  coma  is  usually  preceded  by  uraemic  headaches,  vomiting, 
and  convulsions,  local  or  general.  A  history  of  previous  renal 
disease  is  here  of  great  value.  And  there  may  be  obvious 
signs  of  renal  dropsy  about  the  face  and  legs.  Respiration  is 
frequently  of  the  Cheyne-Stokes  type.  The  breath  often  has  a 
urinous  odour,  and  a  catheter  specimen  of  urine  will  show  albumin 
together  with  various  kinds  of  casts,  and,  in  acute  nephritis, 
blood.  But  we  must  not  forget  that  a  patient  with  chronic 
renal  disease,  a  high-tension  pulse  and  a  hypertrophied  heart,  is 
a  specially  likely  candidate  for  cerebral  haemorrhage.  Therefore 
in  a  case  of  coma,  mere  albuminuria  should  not  lead  us  to 
diagnose  uraemic  coma.  We  must  always  be  on  the  look-out 
for  symptoms  of  unilateral  paralysis. 

Diabetic  Coma  is  easy  to  recognise,  if  we  know  that  the  patient 
has  been  sufiering  from  diabetes.  Even  if  there  be  no  history 
of  diabetes,  examination  of  the  urine  shows  the  characteristic 
high  specific  gravity,  together  with  the  presence  of  sugar  in  large 
amount   as  shown   by   the  ordinary  tests. ^      The  addition  of  a 

^  Glycosuria  by  itself,  however,  is  not  conclusive  evidence  that  a  case  of 
coma  is  diabetic  in  origin,  since  sugar  may  appear  temporarily  in  the  iirine 
as  the  result  of  a  cerebral  lesion  [e.g.  haemorrhage)  or  after  an  epileptic  fit. 
Glycosuria  may  also  occur  as  a  terminal  phenomenon  in  tuberculous  menin- 
gitis, generally  within  the  last  forty-eight  hours  before  death. 


72  NERVOUS    DISEASES 

few  drops  of  liq.  ferri  percUoridi  to  the  urine  produces  a  deep 
brownish-red  colour,  due  to  di-acetic  acid.  The  "  acetone  "  smell 
of  the  breath  is  unmistakable  and  occurs  only  in  diabetes,  in  the 
rare  condition  of  "  delayed  poisoning  by  anaesthetics,"  ^  and  in  the 
"  cyclical  or  periodic  vomiting  "  with  acetonuria  seen  in  children,^ 
both  of  which  latter  conditions  are  associated  with  acute  fatty 
changes  in  the  liver.  Further,  diabetic  coma  is  not  sudden  in  onset, 
but  is  commonly  preceded  by  abdominal  pain,  air-hunger,  and 
uncontrollable  drowsiness,  merging  into  profound  coma  with  re- 
markably deep  breathing.  The  pulse  is  usually  small  and  rapid, 
unlike  the  full,  slow  pulse  of  cerebral  haemorrhage.  Eyeball  ten- 
sion is  usually  lowered  to  a  remarkable  degree.  Rise  of  tem- 
perature, which  is  so  common  in  cerebral  haemorrhage,  does  not 
occur  in  diabetic  coma. 

Sunstroke  sometimes  causes  coma.  Here,  of  course,  for  diag- 
nosis essential  that  there  should  be  a  history  of  exposure  to  a  hot 
sun,  of  a  previously  healthy  patient.  Alcoholic  patients  are  more 
liable  to  sunstroke  than  teetotalers.  A  patient  who  is  comatose 
from  sunstroke  often  has  extraordinary  hyperpyrexia — 108°  F. 
and  upwards.  General  convulsions  may  occur.  The  cerebro- 
spinal fluid  in  such  cases  often  shows  evidences  of  acute  meningeal 
reaction,  in  the  form  of  a  polynuclear  pleocytosis,  passing  on 
subsequently  to  lymphocytosis. 

In  malarial  climates  we  must  also  be  prepared  to  meet  with  a 
comatose  variety  of  pernicious  malaria,  in  which  the  parasites 
produce  thrombosis  of  the  smaller  cortical  vessels.  A  malarious 
patient  may  rapidly  become  comatose  and  die  within  a  few 
hours,  as  happened  to  a  friend  of  my  own.  In  such  cases  the 
malarious  history  and  the  examination  of  the  blood  for  the 
Plasmodium  will  settle  the  diagnosis.  A  patient  dying  from 
cancer  may  become  comatose  shortly  before  death — ^the  so-called 
coma  carcinomatosum. 

We  need  not  do  more  than  mention  the  terminal  coma  of  such 
diseases  as  acute  yellow  atrophy  and  rheumatic  hyper-pyrexia,  or 
the  "  coma- vigil  "  of  typhus  and  of  severe  enteric  fever. 

Hysterical  Trance,  by  a  careless  observer,  might  be  mistaken 
for  true  coma.  The  hysterical  patient,  however,  has  neither  stertor 
nor    cyanosis,    the    breathing    and    heart's    action    are    regular, 

1  Guthrie,  Clinical  Journal,  June  12,  1907. 

^  Langmead,  British  Medical  Journal,  1905,  p.  3C0. 


COMA  7:i 

though  perhaps  very  faint,  the  pupils  react  to  light  and  the  patient 
generally  resists  forcible  opening  of  the  eyes. 

Thus  a  young  man  of  twenty-two  who  had  sudden  attacks  of 
apparent  sleep  (narcolepsy)  coming  on  in  the  middle  of  meals  or 
when  playing  cards,  refused  to  be  roused  by  ordinary  stimidi  in  the 
form  of  shaking  or  shouting,  but  yielded  at  last  to  forcible  digging  in 
the  ribs.  He  passed  through  a  stage  of  "  grande  hysteric"  before 
waking  up,  and  for  some  time  afterwards  had  hysterical  blindness 
and  other  hysterical  stigmata. 

Cases  of  hysterical  trance  constitute  a  fairly  common  variety 
of  war-neurosis.  A  young  soldier,  often  of  neuropathic  diasthesis, 
who  has  had  some  violent  shock,  whether  physical,  from  the 
stunning  effect  of  a  shell-explosion,  or  mental,  from  the  emotion 
produced  by  the  horrors  of  the  battle-field,  is  found  to  be  in  a 
condition  of  trance.  If  placed  in  bed  he  lies  there,  apathetic  and 
silent,  paying  no  attention  to  his  surroundings.  He  does  not  ask 
for  food,  but  if  it  is  placed  in  his  mouth,  he  swallows  it.  He  may 
be  completely  mute  or  he  may  repeat  the  same  word,  or  some 
unintelligible  sound,  over  and  over  again.  If  placed  on  his  feet, 
he  remains  standing,  making  no  efiort  either  to  walk  or  to  get 
into  bed  again.  Sometimes  after  a  few  minutes  his  legs  give  way 
and  he  collapses  on  the  floor,  but  without  hurting  himself.  If  led 
forward  by  the  hand  or  gently  pushed  from  behind,  he  walks  slowly 
with  a  feeble,  shuffling  gait,  but  soon  comes  to  a  standstill.  If 
he  meets  with  an  obstacle,  e.g.  a  wall,  he  remains  in  contact  with  it, 
motionless,  l^his  condition  may  last  from  a  few  days  to  several 
weeks,  clearing  up  gradually  at  first  and  later  somewhat  suddenly. 
The  mutism  often  persists  when  the  other  phenomena  have  dis- 
appeared. The  mute  patient,  nevertheless,  is  able  to  express 
himself  fluently  by  writing.  Sometimes  the  power  of  speech  is 
restored  suddenly,  perhaps  after  some  emotional  shock  of  an 
agreeable  nature.  In  other  cases  the  patient  passes  through  a 
stage  of  severe  stammering,  lasting  for  many  weeks. 

The  hypnotic  trance  may  be  regarded  as  an  artificially-induced 
form  of  hysteria,  the  result  of  suggestion  in  a  sensitive  subject. 


CHAPTER   V 

FITS   AND   OTHER   CONVULSIVE   PHENOMENA 

We  are  often  consulted  about  patients  who  are  said  to  have  "  fits," 
but  we  are  seldom  fortunate  enough  to  witness  an  attack.  If 
we  do,  the  diagnosis  presents  little  difficulty.  More  often,  in 
making  the  diagnosis  as  to  the  nature  of  a  fit,  we  have  to 
depend  upon  the  description  given  by  the  patient's  friends. 

The  following  is  a  list  of  the  chief  clinical  conditions  in  which 
convulsive  phenomena  occur  : — 

r  Hysteria  major. 
J  Catalepsy. 
1  Hysteria  minor. 
I  Post-epileptic  hysterical  attacks. 

Epilepsy  major  (grand  vial). 
Epilejjsy  minor  (petit  mal). 
Post-epileptic  automatism — "  masked 

epilepsy." 
Toxic     conditions  : — Asphyxia,    urse- 
mia,  puerperal  eclampsia,  alcohol, 
Epileptiform  (       absinthe,  lead,  &c. 

'  General  paralysis  of  the  insane. 
Psychasthenia. 

Organic     brain     lesions — Jacksonian 
fits,  &c. 

r  Toxic. 


Hysterical 


CEREBRAL  FITS  J 


Infantile  Convulsions 
Stokes-Adams'  disease. 


\  Organic. 


CEREBELLAR  FITS. 


In  making  inquiries  about  convulsive  phenomena,  whatever 
their  nature,  it  is  advisable  to  avoid  using  the  word  "  fit," 
especially  if  we  are  discussing  symptoms  in  the  presence  of  the 
patient.  It  is  better  to  refer  simply  to  "  attacks."  Many 
epileptics  are  unaware  of  their  own  disease,  and  even  when  they 
know  its  nature,  they  dislike  hearing  about  their  "  fits." 

The  first  point  we  should  try  to  determine  is  whether  the 

74 


F1T8    AND    OTHKR    CONVULSIVE    PHENOMENA     75 

attacks  are  hysterical  or  epileptiform.  In  reference  to  this  the 
age  and  sex  of  the  patient  are  often  of  importance.  We  do  not 
meet  with  hysteria  in  infants,  and  rarely  in  children  below  the 
age  of  puberty.  Epilepsy  is  of  equal  frequency  in  both  sexes, 
whereas  hysteria  is  twenty  times  commoner  in  females  than  in 
males.  Hysterical  attacks  in  male  patients  are  most  frequent  in 
lads  at  about  the  age  of  puberty. 

Scheme  of  Investigation  in  Cases  of  Fits 

Exciting  cause.  Nature  of  warning,  if  any.  Onset,  sudden  or  gradual. 
Scream.  Injuries  during  falling.  Movements,  tonic,  clonic,  purposive. 
Starting-point  of  movements,  and  exact  order  of  spread.  Biting  of  tongue. 
Micturition  or  defsecation.  Colour  of  face,  pale,  flushed,  c3-anosed.  Pupils. 
Corneal  reflexes.  Knee-jerks  immediately  after  attack.  Duration  of  attack. 
After-symptoms  (coma,  vomiting,  headache,  sleep,  &c.). 

Pursuing  the  foregoing  scheme,  we  should  inquire  whether 
there  was  any  apparent  cause  for  the  attack.  Hysterical  attacks 
generally  follow  some  emotional  disturbance.  Epilepsy  comes  on 
without  exciting  cause.  A  warning  or  aura  before  an  attack 
of  epilepsy  may  be  of  the  most  varied  character.  Perhaps 
the  commonest  is  the  "  epigastric "  aura,  or  there  may  be 
an  indescribable  feeling  of  terror,  subjective  auditory  or  visual 
phenomena  (visual  aurse  being  most  frequently  red  in  colour), 
unilateral  tingling  or  twitching  of  the  face  or  one  of  the  hmbs,  or 
a  "  dreamy  "  mental  state  (sometimes  associated  with  subjective 
sensations  of  smell  or  taste),  and  so  on,  according  to  the  particular 
cortical  area  whence  the  epileptic  explosion  happens  to  start.  But 
often  the  epileptic  has  no  aura ;  he  falls  suddenly  as  if  struck 
down  by  an  unseen  hand.  If  we  happen  to  be  feehng  the  pulse 
of  an  epileptic  at  the  moment  of  onset  of  a  fit,  it  will  sometimes  be 
noticed  that  the  heart  suddenly  stops  for  a  few  seconds.  Such 
cardiac  arrest,  however,  is  not  invariable.  Hysterical  attacks 
usually  come  on  gradually,  and  are  often  preceded  by  the  hysteri- 
cal "  globus  "  or  ball  in  the  throat,  or  by  feelings  of  palpitation, 
excitement,  giddiness,  tingling  in  the  feet,  &c.  Sometimes  at  the 
onset  of  the  attack  t  he  epileptic,  as  he  falls,  utters  a  weird  epileptic 
cry  or  moan,  which  is  not  repeated.  By  this  time  he  is  already 
unconscious  and  does  not  hear  his  own  cry.  Frequently  he  injures 
himself  in  falling  especially  by  striking  his  head.  Many  chronic 
epileptics  may  be  recognised  by  the  presence  of  numerous  scars 
on  the  scalp   and  face.     The  hysterical  patient,  on  the  contrary, 


76  NERVOUS    DISEASES 

never  injures  herself  when  fahing.  She  comes  down  carefully, 
often  on  a  sofa  or  easy-chair.  She  not  uncommonly  screams,  and 
may  continue  to  scream  or  shout  throughout  the  attack. 

The  nature  of  the  movements  during  the  attack  is  of  importance. 
In  epilepsy  we  have  the  tonic  stage,  in  which  all  the  voluntary 
muscles,  including  those  of  respiration,  become  suddenly  rigid. 
The  patient,  therefore,  falls  like  a  log,  and  his  lips  and  face  become 
cyanosed,  his  pupils  dilating  and  becoming  insensitive  to  light. 
The  tonic  stage  passes  into  the  clonic,  in  which  violent  jerking 
occurs  in  all  the  voluntary  muscles,  at  first  rapid,  and  gradually 
becoming  slower  and  of  greater  range.  The  eyes,  which  during 
the  tonic  stage  have  been  drawn  to  one  side  (the  side  on  which 
the  tonic  spasm  was  more  intense),  now  show  rapid  clonic  jerks 
towards  that  side  and  the  mydriasis  ceases.  The  face  loses  its 
cyanotic  hue,  air  re-enters  the  lungs,  and  is  jerked  out  in  short 
puffs  mixed  with  saliva,  forming  a  froth  which  is  not  infrequently 
blood-stained,  since  the  jerking  tongue  may  be  bitten  by  the 
clonic  movements  of  the  jaws.  During  this  stage  the  patient  often 
empties  the  bladder  and  sometimes  the  rectum.  Within  two  or 
three  minutes  from  their  onset  the  movements  gradually  cease, 
and  the  patient  remains  in  a  state  of  coma,  with  stertorous 
breathing,  flaccid  limbs,  and  sometimes  profuse  sweating,  the 
eyes  being  now  turned  to  the  side  opposite  to  that  towards 
which  they  originally  deviated,  and  the  pupils  being  now  con- 
tracted. Then,  after  ten  minutes  or  so,  the  coma  passes  off,  and 
the  patient  may  vomit,  or  may  wake  up,  perhaps  with  a  headache, 
or  may  pass  into  a  sound  sleep. 

In  a  hysterical  attack,  on  the  other  hand,  the  patient's  face 
is  natural  in  colour,  never  cyanosed,  though  later  it  may  become 
flushed  from  physical  exertion.  The  voluntary  muscles  are  usually 
contracted,  the  fists  clenched,  the  eyes  tightly  closed  and  resistant 
to  opening,  but  if  the  eyes  be  forcibly  opened  the  eyeballs  roll 
upwards.  Then,  after  a  stage  of  general  tremor  totally  unlike  the 
clonic  stage  of  epilepsy,  the  patient  makes  violent  "  purposive  " 
movements,  kicking,  pushing,  biting,  rolling  about,  banging  her 
head  on  the  floor,  beating  her  own  face,  pulling  her  hair,  &c. 
During  this  stage  various  grotesque  postures  may  be  assumed  ;  of 
thes3,  the  most  characteristic  is  one  in  which  the  back  is  arched 
(opisthotonos)  and  the  patient  rests  on  her  head  and  heels.  Or 
there   may  be   curving   of  the  trunk  laterally  (pleurosthotonos), 


FITS    AND    OTHER    CONVULSIVE    PHENOMENA     77 

or  forwards  (emprosthotonos),  "  crucifixion "  attitude,  &c.  The 
patient  may  talk,  scream,  or  sing  during  the  attack,  which  may  last 
for  many  minutes.  But  throughout  the  attack  the  pupils  generally 
react  to  light,  and  the  corneal  reflex  is  usually  preserved.  The 
hysterical  patient  never  bites  her  tongue,  though  she  may  bite  her 
lips  or  fingers,  or  snap  at  the  fingers  of  bystanders.  She  never 
empties  the  bladder  or  rectum  during  the  attack,  and  after  it  is 
over  she  may  or  may  not  have  any  recollection  of  what  has 
happened,  and  is  sometimes  in  a  semi-dazed  condition.  The 
hysterical  patient  is  more  likely  to  recover  suddenly  after  the 
fit  than  the  epileptic ;  also  she  is  more  likely  to  "  feel  better '' 
after  the  fit  than  in  the  case  of  an  epileptic. 

The  knee-jerks,  during  the  stage  of  flaccid  coma  terminating  a 
severe  epileptic  fit,  may  be  temporarily  aboUshed,  but  soon  they 
become  exaggerated,  and,  for  a  few  minutes,  ankle-clonus  may 
often  be  elicited,  and  the  plantar  reflex  may  be  extensor  in  type. 
In  hysteria  the  deep  reflexes  are  unaltered. 

If  we  bear  in  mind  the  foregoing  points,  the  diagnosis  between  a 
severe  epileptic  fit  and  an  Sittsickoi"  grande  7i?/s;;me"  is  generally  easy. 

Catalepsy,  another  variety  of  hysterical  attack,  is  easily  recog- 
nised by  the  peculiar  immobility  of  the  limbs.  The  patient  during 
the  attack,  though  not  unconscious,  is  unable  to  move  a  muscle, 
but  her  limbs  are  plastic  like  those  of  a  lay  figure,  and  if  placed 
passively  in  any  posture,  remain  there. 

There  are  also  many  varieties  of  minor  hysterical  attacks,  easy 
of  recognition,  of  which  the  commonest  consist  merely  in  emotional 
outbursts  of  uncontrollable  laughing  or  crying,  or  a  feeHng  of  a 
lump  in  the  throat — "  globus  hystericus  " — which  causes  the  patient 
to  swallow. 

Supposing,  then,  that  we  have  come  to  the  conclusion  that 
the  patient's  attacks  are  hysterical  and  not  epileptiform,  we  should 
not  rest  content  until  we  have  settled  the  further  point  as  to 
whether  the  hysterical  attack  was  preceded  by  an  attack  of 
minor  epilepsy  or  petit  mal. 

Attacks  of  petit  mal  are  often  overlooked.  It  is  well  to 
remember  that  in  true  epilepsy  (whether  major  or  minor)  the  one 
essential  phenomenon  is  not  convulsions  but  loss  of  consciousness. 
In  petit  mal  it  may  be  the  only  phenomenon,  so  transient, 
perhaps,  that  the  patient  does  not  even  fall ;  he  simply  pauses 
for  an  instant  during  conversation,  lookg  strange,  and  then  goes 


78  NERVOUS    DISEASES 

on  with  what  he  was  saying.  Or  he  may  fall  down  and  get 
up  again  immediately,  a  variety  of  epilepsy  which  is  often  mis- 
taken for  sjnicope,  but  is  distinguished  by  the  suddenness  of 
onset  and  of  recovery.  If  we  happen  to  observe  a  patient  at  the 
moment  of  his  attack  of  fetit  mal,  we  generally  notice  that  the 
pupils  dilate  and  his  face  turns  momentarily  pale,  the  pallor  being 
followed  by  flushing.  It  is  immediately  after  such  a  minor  attack 
that  some  patients  go  on  to  a  'post-efileftic  hysterical  attack,  and  if 
the  initial  epilepsy  be  not  recognised,  treatment  will  fail. 

Attacks  of  minor  epilepsy  are,  now  and  then,  associated  with 
post- epileptic  automatism,  in  which  the  patient  has  an  attack  of 
petit  mal  which  perhaps  passes  unnoticed  ;  he  then  proceeds  to 
perform  some  unusual  or  inappropriate  act,  of  which  he  has  no 
recollection  afterwards.  Perhaps  the  commonest  automatic  action 
is  that  of  undressing ;  or  he  may  proceed  to  empty  his  bladder,  as 
in  the  oft-quoted  instance  of  the  judge  who  did  so  in  the  corner  of 
his  court  of  justice  ;  or  he  may  perform  some  still  more  complicated 
action.  Thus  a  case  of  mine  was  that  of  a  well-known  financier 
who  had  several  attacks  of  loss  of  memory.  During  one  of  these, 
lasting  two  and  a  half  hours,  he  attended  an  important  board- 
meeting  and  proposed  certain  resolutions  to  which,  both  before 
and  after,  he  was  strongly  opposed.  He  then  took  a  friend  out  to 
lunch  and  returned  to  his  office.  He  finally  woke  up  and  asked 
his  confidential  clerk  where  he  had  been.  The  medico-legal  signi- 
ficance of  these  cases  is  of  importance,  since  such  a  patient,  in  a 
condition  of  post-epileptic  automatism,  may  commit  serious  and 
complicated  crimes,  of  which  he  has  afterwards  no  recollection. 
This  condition  is  sometimes  called  "  masked  "  or  "  larval  "  epilepsy. 
It  is  possible  that  attacks  of  automatism  or  psychic  epilepsy  may 
occasionally  actually  replace  the  ordinary  epileptic  fit  without 
an  antecedent  attack  of  petit  mal,  may  in  fact  be  "  epileptic  equi- 
valents." But  the  more  carefully  such  cases  are  observed,  the 
oftener  is  some  indication  found  of  minor  epilepsy  immediately 
before  the  eccentric  action,  in  the  form  perhaps  of  initial  transient 
pallor.  This  was  so  in  the  case  of  the  financier  above  referred  to. 
Other  cases  of  ambulatory  automatism  are  hysterical  in  nature 
(see  later,  p.  402).  A  previous  history  of  epilepsy,  either  major  or 
minor,  is  of  great  diagnostic  value. 

Supposing  that,  having  excluded  hysteria,  we  arrive  at  the 
conclusion  that  a  patient's  fits  are  epileptiform,  we  must  still  re- 


FITS    AND    OTHER    CONVULSIVE    PHENOMENA     79 

member  that  other  conditions  besides  idiopathic  epilepsy  can  pro- 
duce epileptiform  fits.  Sudden  obstruction  of  the  larynx,  e.g.  by 
a  piece  of  meat,  bolted  in  a  hurry,  becoming  impacted  at  the  top 
of  the  larynx,  may  cause  immediate  unconsciousness  followed  by 
a  typical  epileptiform  fit  and  by  death  unless  the  offending  foreign 
body  be  promptly  extracted.  Similar  as'phyxial  fits  sometimes 
occur  in  cases  of  attempted  suicide  by  hanging,  where  the  uncon- 
scious person  is  cut  down  in  time.  Fits  may  also  be  of  toxic 
origin.  Acute  alcoholic  or  absinthe  poisoning  may  produce  coma 
and  convulsions.  The  history  and  the  smell  of  the  breath  will 
usually  guide  us  in  such  cases.  The  sudden  withdrawal  of 
alcohol  from  a  chronic  drunkard  is  sometimes  followed  by  an 
epileptiform  fit.  In  patients  suffering  from  the  convulsions  of 
lead  poisoning  there  are  usually  some  of  the  other  signs  of  plumbism, 
such  as  the  blue  line  in  the  gums,  high  arterial  tension,  weakness 
of  the  extensors  of  the  wrist,  optic  neuritis,  &c.,  whilst  the  cerebro- 
spinal fluid  shows  a  lymphocytosis.  Toxins  produced  within  the 
body  may  also  cause  fits  exactly  similar  to  epilepsy,  witness  the 
urcemic  convulsions  of  Bright 's  disease  and  of  puerperal  eclampsia. 
In  every  case  of  fits  appearing  in  a  previously  healthy  individual, 
the  urine  should  be  tested  and  the  optic  discs  examined.  In  the 
case  of  a  young  officer  who  was  brought  into  hospital  at 
Pretoria  suffering  from  a  succession  of  fits  typically  epileptic  in 
character,  acute  nephritis  was  the  cause.  In  chronic  renal 
disease,  besides  the  cardio -vascular  changes,  there  not  uncommonly 
exists  albuminuric  retinitis,  which  is  of  great  diagnostic  significance. 
When  we  come  to  the  subject  of  infantile  convulsions  we  shall  find 
that  many  of  them  are  toxic  in  origin. 

Epileptiform  fits  may  occur  during  the  course  of  general  paralysis 
of  the  insane  ;  they  may,  in  fact,  be  the  first  symptom  of  the 
disease.  Epileptic  fits  appearing  for  the  first  time  in  a  middle- 
aged  patient  should  always  suggest  the  possibility  of  paralytic 
dementia.  In  such  cases  we  look  for  inequality  or  irregularity  of 
the  pupils,  and  especially  loss  of  the  light  reflex,  mental  changes, 
facial  tremors,  and  slurring  articulation,  and  a  history  of  syphihs 
should  be  sought.  Lumbar  puncture  will  show  lymphocytosis 
of  the  cerebro-spinal  fluid,  a  condition  which  is  constant  in  general 
paralysis  but  does  not  occur  in  idiopathic  epilepsy. 

Epileptiform  or  hystero-epileptiform  fits  may  also  occur  in 
psychasthenic  individuals.     Such  patients  have  stigmata  of  psych- 


80  NERVOUS    DISEASES 

asthenia  in  the  form  of  phobias,  tics,  obsessions,  &c.  (see  p.  381). 
Epileptiform  fits  in  psychasthenia,  unlike  true  epilepsy,  occur  only 
after  some  direct  exciting  cause,  such  as  physical  or  mental  over- 
exertion, excitement,  &c.  The  attacks,  as  a  rule,  are  few  in  number 
and  may  be  limited  to  a  single  one. 

Intra-cranial  tumours  anywhere,  even  deep  within  the  substance 
of  the  brain,  may  cause  general  epileptiform  fits,  from  increased 
intra-cranial  pressure.  Here  we  are  usually  guided  by  the  cardinal 
signs  of  intia-cranial  tumour— headache,  vomiting,  optic  neuritis,  &c. 

All  the  epileptiform  fits  to  which  we  have  as  yet  alluded  have 
a  bilateral  general  distribution,  and  are  not  succeeded  by  any 
localised  paralysis.  But  when  fits  are  produced  by  gross  focal  irrita- 
tion of  the  cortex  their  onset  is  a  local  one,  and  they  are  not 
necessarily  associated  with  loss  of  consciousness.  Such  "  Jack- 
sonian  fits  "  are  usually  followed  by  weakness  of  the  part  which 
is  primarily  convulsed.  Jacksonian  fits  may  occur  as  often  as 
fifty  or  a  hundred  times  a  day.  They  usually  begin  with  a 
subjective  sensory  aura,  such  as  tingling,  numbness  or  twitching, 
localised  in  some  particular  part,  e.g.  the  thumb  or  big  toe.  Then 
there  is  tonic  spasm  of  that  part,  followed  by  clonic  jerking. 
This  may  remain  confined  to  the  muscles  where  it  began,  or 
it  may  spread  to  others.  If  it  spreads,  it  does  so  by  a 
deliberate  march  from  one  cortical  centre  to  another  (Fig.  3,  p.  5). 
Thus  a  fit  commencing  in  the  big  toe  would  occur  successively 
in  the  ankle,  knee,  hip,  shoulder,  elbow,  hand,  &c.,  and  would 
affect  the  face  last  of  all.  Or  a  fit  beginning  in  the  elbow  would 
spread  via  the  shoulder,  hip  and  knee,  to  the  toes,  and  simul- 
taneously vid  the  wrist,  fingers  and  neck,  to  the  face  and  tongue, 
as  the  ripples  produced  by  dropping  a  stone  into  a  pool  spread 
in  ever- widening  circles.  A  patient  who  has  Jacksonian  fits 
may  remain  conscious  throughout  the  fit  and  may  even  be  able 
to  speak,  though  he  is  usually  somewhat  confused  and  excited. 
But  if  the  convulsion  spreads  to  the  opposite  cortical  area,  thus 
becoming  bilateral,  consciousness  is  lost  as  the  fit  crosses  over. 
Jacksonian  fits  are  followed  by  local  weakness  and  increased  deep 
reflexes  in  the  convulsed  part.  Fig.  37  shows  a  patient  during 
a  locahsed  fit  in  the  left  face,  due  to  a  gumma  in  the  cortical  facial 
centre.  Fig.  38  shows  the  maximum  voluntary  movement  of  the 
face  after  an  attack.  It  will  be  seen  that  the  left  lower  face 
is  markedly    weaker    than    the    right.      The    locahsed    paralysis 


FITS    AND    OTHER    CONVULSIVE    PHENOMENA      81 

passes  off  in  the  reverse  order  from  that  in  which  the  spasm 
appeared,  the  muscles  first  convulsed  being  the  last  to  recover 
power. 

Of  course,  cortical  lesions  will  produce  localised  motor  pheno- 
mena only  if  they  affect  the  motor  centres  in  the  region  of  the 
pre-central  gyrus.  A  focal  lesion  of  a  sensory  cortical  area  pro- 
duces, not  a  motor,  but  a  sensory  fit.  Thus  disease  of  the  tip 
of  the  temporal  lobe  (Fig.  4,  p.  5)  causes  a  sudden  subjective 
sensation  of  smell  or  taste  (often  associated  with  a  characteristic 
"  dreamy  "  mental  state) ;   occipital  lesions  cause  subjective  visual 


Fig.  37.  Fig.  38. 

Cortical  gumma  of  the  face-centre  of  the  right  cerebral  cortex. 

Fig.  S7  shows  patient  during  a  Jacksonian  fit  of  the  left  face. 
Fig.  38  shows  weakness  of  the  left  face  on  voluntary  movement. 

hallucinations  such  as  flashes  of  light ;  and  so  on.  Moreover,  after 
the  sensory  fit  it  is  not  uncommon  to  find  temporary  sensory 
paralysis,  e.g.  anosmia  after  a  temporal  fit,  or  hemianopia  after 
an  occipital  fit. 

A  Jacksonian  fit,  of  whatever  variety,  is  the  result  of  a  local 
lesion  in  the  neighbourhood  either  of  the  cortex  or  of  its  superjacent 
meninges  or  bones.  If  the  lesion  be  in  the  substance  of  the  cortex, 
not  merely  superficial  to  it,  there  is  often  some  local  paralysis  even 
before  the  fit  occurs. 

Localised  fits  may  be  produced  by  any  irritative  cortical  lesion. 
The  commonest  causes  are  tumours,  syphilitic  or  otherwise,  ab- 
scesses, meningitis  of  any  variety,  local  hsemorrhages,  depressed 
fractures,  and    so   on.     Localised  fits  may  also  be  produced  by 

F 


82  NERVOUS    DISEASES 

s'vA>- cortical  tumours  in  the  pre-central  region.  In  such  cases 
we  observe  muscular  paresis  in  the  affected  Hmb,  together  with 
recurring  convulsive  phenomena  in  the  limb  ;  but  the  point  of 
onset  of  the  successive  fits  is  less  constant  than  in  a  true  cortical 
convulsion,  and  the  fit  begins  sometimes  in  one,  sometimes  in 
another  muscle-group  of  the  affected  limb.^  We  should  also  bear 
in  mind  that  Jacksonian  fits  may  occur  in  certain  cases  of  general 
paralysis  of  the  insane,  and  sometimes  even  in  uraemia. 

Infantile  Convulsions  are  epileptiform  attacks  occurring  in 
infancy.  The  symptoms  are  similar  to  those  of  true  epilepsy,  but 
less  violent.  When  called  to  see  a  child  with  convulsions,  we 
should  first  examine  for  rickets,  since  rickety  and  hereditarily 
neurotic  children  are  especially  prone  to  convulsions.  We  should 
also  try  to  determine  whether  the  fits  are  reflex,  toxic,  or  organic 
in  origin.  In  rickety  infants  of  neurotic  inheritance  reflex  convul- 
sions may  be  set  up  by  peripheral  irritation  such  as  the  cutting  of  a 
tooth,  round-worms  in  the  intestine  (thread-worms  do  not  cause 
convulsions),  a  tight  prepuce,  &c.  Moreover,  rickety  children  often 
have  other  evidences  of  spasmophilia,  such  as  tetany,  laryngismus 
stridulus,  and  the  well-known  inversion  of  the  thumbs  towards 
the  palms,  a  phenomenon  which  sometimes  precedes  a  convulsion. 
Toxic  conditions  may  produce  convulsions  in  previously  healthy 
children.  Thus  any  acute  fever  such  as  pneumonia,  measles,  scarlet 
fever  or  influenza,  may  be  ushered  in  by  a  convulsion  instead  of 
by  a  rigor  as  in  the  adult.  The  convulsions  produced  by  round- 
worms may  be  partly  toxic  in  origin.  Uraemic  convulsions  occur 
in  children,  though  less  often  than  in  adults,  and  in  cases  with 
recurring  convulsions  the  urine  should  always  be  examined. 
Asphyxial  convulsions,  due  to  deficient  oxygenation  of  the  brain, 
occur  in  dyspnoea  from  any  cause,  e.g.  during  pneumonia  and 
diphtheria,  during  a  paroxysm  of  whooping-cough,  or  in  the 
cyanosis  of  congenital  heart  disease.  Intra-cranial  organic  lesions 
may  cause  infantile  convulsions.  Thus,  for  example,  polio-ence- 
phalitis superior,  an  acute  inflammatory  affection  of  the  cortex, 
has  a  febrile  onset  with  vomiting  and  convulsions,  usually  more 
marked  on  one  side  than  on  the  other.  After  the  convulsions 
have  passed  off,  the  child  is  often  left  permanently  hemiplegic  or 
diplegic.  If  the  cortex  of  the  frontal  region  is  affected,  permanent 
mental  dulness  may  remain.     The  nuclei  of  various  motor  cranial 

1  Gf.  van  Valkenburg,  Neurologisches  Centralblatt,  1906,  p.  594. 


FITS    AND    OTHER    CONVULSIVE    PHENOMENA     83 

nerves  may  also  be  affected  (polio-encephalitis  inferior),  producing 
squint,  facial,  palatal,  or  glossal  palsy.  The  coexistent  meningeal 
inflammation  is  evidenced  by  a  lymphocytosis  of  the  cerebro- spinal 
fluid.  It  is  sometimes  difiicult  to  distinguish  the  disease  from 
tuberculous  meningitis.  In  polio-encephalitis,  however,  the  coma 
is  usually  less  profound  and  the  disease  is  much  less  fatal.  More- 
over, the  cerebro- spinal  fluid,  although  showing  a  lymphocytosis, 
does  not  contain  tubercle  bacilli. 

Local  disease  or  injury  of  the  bones  or  membranes  may  produce 
infantile  convulsions.  Convulsions  appearing  within  a  few  hours 
after  birth  are  not  unfrequently  the  result  of  compression  of  the 
brain  by  a  meningeal  haemorrhage  of  venous  origin  from  laceration 
of  cortical  veins.  In  such  cases  the  diagnosis  may  be  confirmed 
by  examining  the  cerebro-spinal  fluid,  which  is  blood-stained. 

Meningitis,  whether  due  to  the  tubercle  bacillus,  to  syphilis, 
or  to  other  organisms,  may  produce  convulsions,  not  only  when 
cortical,  in  which  case  convulsions  appear  early,  but  also  in 
basal  oases,  where  the  fits  are  due  to  increased  intra-cranial 
pressure. 

Epileptiform  fits  also  occur  in  one  variety  of  the  Stokes-Adams' 
syndrome,  a  condition  which  occurs  after  middle  life,  usually  in 
male  patients  with  degenerate  arteries,  and  is  characterised 
by  paroxysmal  attacks  of  abnormal  slowness  of  the  ventricular 
beat,  the  rate  sinking  as  low  as  twenty  per  minute  or  even  less, 
together  with  excessive  pulsation  in  the  veins  at  the  root  of  the 
neck,  more  rapid  than  the  ventricular  beats,  and  corresponding 
with  the  auricular  contractions.  Such  a  patient  is  liable  to 
syncopal  attacks,  to  which  may  be  superadded  epileptiform  fits 
or  attacks  of  coma  without  convulsions.  Fits  do  not  occur  unless 
the  heart-block  is  complete,  where  the  ventricle  no  longer  responds 
to  auricular  stimulation.  More  or  less  slowness  of  pulse  usually 
persists  between  the  paroxysms,  as  a  permanent  phenomenon. 
The  condition  is  frequently  due  to  disease,  syphilitic  or  otherwise, 
of  the  auriculo-ventricular  muscle-bundle  of  Stanley  Kent  ^  and 
His,  which  arises  in  the  right  auricle,  traverses  the  inter- ventri- 
cular septum  and  is  distributed  to  both  ventricles.  When  this 
bridge  is  diseased,  the  normal  stimulus  from  auricle  to  ventricle 
is  delayed  or  may  even  be  completely  blocked.  This  is  known 
as  heart-block,  in  which  the  auricles  go  on  contracting  normally, 

1  Kent,  Journal  of  Physiology,  1893,  vol.  xiv.  p.  233. 


84  NERVOUS    DISEASES 

but  the  ventricle  only  responds  to  every  second  or  every  third 
stimulus.  There  is  thus  a  dissociation  between  auricular  and 
ventricular  rhythm.^ 

Strychnine  Convulsions  should  never  be  confounded  with 
epileptiform  fits,  since  they  begin  with  clonic  spasms,  and 
shortly  become  tonic  with  opisthotonos,  the  tonic  spasms  recurring 
again  and  again  with  increasing  severity.  A  patient  poisoned  by 
strychnine  is  not  unconscious.  Moreover,  there  are  periods  of 
intermission,  lasting  for  several  minutes  at  a  time,  during  which 
the  muscles  are  relaxed. 

The  tonic  spasms  of  tetanus  might  be  mistaken  for  strychnine- 
poisoning,  but  they  have  no  initial  clonic  stage.  The  earliest 
symptom  of  tetanus  is  the  well-known  tonic  spasm  of  the  jaw 
muscles,  producing  "  lock-jaw."  To  this  there  are  superadded 
paroxysms  of  tonic  spasm  in  the  face  {risus  sardonicus),  trunk 
and  limbs,  with  opisthotonos,  somewhat  like  those  of  the  tonic 
stage  of  strychnine-poisoning.  Between  the  tetanic  paroxysms 
there  is  no  complete  muscular  relaxation  as  in  strychnine-poisoning, 
but  simply  a  remission  in  the  degree  of  spasm,  the  jaw  muscles 
remaining  partially  contracted. 

A  patient  suffering  from  ra"bies  exhibits  great  mental  excite- 
ment, often  amounting  to  acute  dehrious  mania,  with  tonic  spasm 
of  the  muscles  of  deglutition,  especially  on  attempting  to  swallow 
liquids  (hence  the  misnomer  hydrophobia).  Unswallowed  saliva 
may  ooze  from  the  mouth.'  The  spasm  may  also  be  induced  by 
other  stimuli  such  as  a  bright  hght  or  a  loud  sound.  The  spasm 
spreads  to  other  muscles,  especially  those  of  respiration,  and  severe 
opisthotonos  may  supervene  at  the  end,  the  patient  dying  either 
of  respiratory  spasm  or  from  syncope.  Hydrophobia  may  be 
simulated  by  hysterical  patients  who  have  been  bitten  by  a  non- 
rabid  dog,  and  in  such  cases  globus  hystericus  and  hysterical 
opisthotonos  may  both  occur,  but  true  respiratory  spasm  does  not 
occur  in  hysterical  attacks,  though  there  may  be  hysterical  rapidity 
of  breathing. 

During  an  attack  of  tetany  the  posture  is  very  characteristic. 
There  is  a  bilateral  tonic  spasm,  usually  painful,  of  the  hands  and 
feet,  the  hand  assuming  a  conical  shape  ("  main  d' accoucheur  "),  the 
fingers  being  extended  at  the  inter-phalangeal  joints,  slightly  flexed  at 
the  metacarpo-phalangeal  joints  and  pressed  together  with  the  thumb 

1  Mackenzie,  Diseases  of  the  Heart,  1908,  p.  169. 


FITS    AND    OTHER    CONVULSIVE    PHENOMENA      85 

usually  tucked  inside  the  fingers  ;  at  the  same  time  the  muscles  of  the 
thenar  and  hypothenar  eminences  are  contracted,  so  that  the  hollow 
of  the  palm  is  deepened.  In  the  feet,  the  toes  are  flexed  towards  the 
sole,  the  ankle  is  dorsiflexed  and  the  foot  is  sometimes  inverted. 
These  postures  may  persist  during  sleep.  Pressure  on  the  nerve- 
trunks  of  the  affected  limb  induces  a  typical  spasm  (Trousseau's 
sign),  and  the  muscles  and  nerves  are  unduly  irritable  both  to  fara- 


FiG.  39.— Tetany. 


dism  and  to  galvanism  (Erb's  sign).  Tetany  is  most  commonly  met 
with  in  rickety  children  (Fig.  39)  with  deficiency  of  calcium  salts, 
in  whom  it  is  often  associated  with  other^evidences'^of  "  spasmo- 
philia "  such  as  laryngismus  stridulus  and  excessive  irritability  on 
percussion  of  the  facial  nerve  (Chvostek's  facial  phenomenon). 
But  it  occasionally  occurs  in  adults,  e.g.  after  extirpation  of  the 
thyroid  gland,  or  rather  of  the  parathyroids,  whose  internal  secre- 
tion plays  an  important  part  in  maintaining  a  sufficiency  of  calcium 
salts  in  the  tissues.     Tetany  is,  therefore,  sometimes  a  symptom 


86 


NERVOUS    DISEASES 


of  parathyroid  deficiency,  whether  arising  from  disease  or  from 
artificial  removal  of  the  glands.  Tetany  also  occm's  sometimes 
during  pregnancy  or  lactation,  and  as  a  grave  terminal  symptom 
in  dilatation  of  the  stomach.  This  variety  of  tetany  is  probably 
toxic  in  origin  :  so  also  are  the  rare  cases  of  tetany  associated  with 
congenital  dilatation  of  the  large  intestine  in  children.-^  Cataract 
is  a  curiously  frequent  concomitant  of  the  gastric  form  of  tetany. 
An  endemic  form  of  tetany  also  occurs  in  certain  Continental 
towns,  chiefly  in  the  winter  months.  It  is  especially  common 
amongst  shoemakers. 

Cerebellar  Fits. — Irritative  lesions  of  the  sub-cortical  intra- 


FiG.  40. — Chvostek's  sign  of  Tetany  on  percussion  over 
the  right  facial  nerve. 


cerebellar  nuclei  are  occasionally  associated  with  cerebellar  fits. 
These  are  never  clonic,  but  consist  of  tonic  spasms,  sudden  in 
onset.  In  unilateral  cerebellar  disease  the  spasms  are  more  marked, 
in  the  ipso-lateral  limbs  than  in  those  of  the  opposite  side.  The 
face  is  usually  unaffected.  The  ipso-lateral  limbs  become  rigidly 
adducted  to  the  trunk,  the  contra-lateral  limbs  are  abducted,  whilst 
at  the  same  time  there  is  a  screw-like  rotation  of  the  limbs,  trunk 
and  head  around  their  own  long  axes,  from  the  side  of  the  lesion 
towards  the  healthy  side,^  and  a  deviation  of  the  eyes  towards 
the  healthy  side.  HughUngs  Jackson  has  described  another  variety 
of  cerebellar  fit  occurring  in  cases  of  tumour  of  the  middle  lobe. 

^  Langmead,  Lancet,  Jan.  19,  1907. 

-  Grainger  Stewart  and  Holmes,  Brain,  1904. 


FITS    AND    OTHER    CONVULSIVE    PHENOMENA     87 

Here  also,  as  in  tumours  of  the  lateral  lobe,  the  fits  are  tonic,  not 
clonic.  They  consist  of  head-retraction  with  arching  of  the  back, 
flexion  of  the  elbows,  supination  of  the  hands,  and  rigid  extension 
of  the  legs,  with  pointing  of  the  toes. 

But  let  us  not  forget  that  epileptiform  fits  of  cerebral  type 
may  also  occur  in  cases  of  cerebellar  tumour,  due  either  to  the 
general  increase  of  intra-cranial  pressure,  or  to  a  fulminating 
meningitis  superadded  to  an  old  tuberculous  tumour. 


CHAPTER   VI 

INVOLUNTARY   MOVEMENTS 

Besides  fits,  which  we  have  already  considered,  there  are  many 
other  conditions  in  which  involuntary  contractions  occur  in 
the  voluntary  muscles.  But  our  knowledge  of  the  mechanism 
of  their  causation  is  so  incomplete  that  it  is  impossible 
at  present  to  classify  them  accurately.  We  must  therefore 
content  ourselves,  in  the  meanwhile,  with  referring  to  some  of 
their  chief  clinical  varieties. 

In  studying  involuntary  movements  occurring  in  striated 
muscles,  it  is  important  to  observe  whether  the  movement  is  con- 
fined to  an  individual  muscle  or  part  of  a  muscle,  or  whether,  on 
the  other  hand,  it  consists  in  alternate  contraction  of  muscles  and 
of  their  antagonists.  We  should  also  observe  whether  the  abnormal 
muscular  contractions  produce  movements  of  a  joint,  or  whether 
they  are  so  localised,  either  to  a  small  muscle  or  to  part  of  a 
larger  one,  that  we  merely  see  or  feel  the  muscle  fibres  contracting 
beneath  the  skin. 

The  muscular  phenomenon  known  as  shivering  or  rigor  is  some- 
times physiological.  For  example,  when  a  healthy  person  becomes 
chilled,  as  by  prolonged  swimming,  he  often  shiveis  on  coming 
out  of  the  water.  The  involuntary  muscular  contractions  of 
which  shivering  consists  are  for  the  purpose  of  producing  heat 
and  thereby  raising  the  depressed  body-temperature.  But  often 
rigors  are  toxic  in  origin,  as  are  those  occurring  at  the  onset  of 
certain  acute  fevers.  Thus  we  have  rigors  in  pneumonia,  ague, 
influenza,  scarlet  fever,  &c.  And  the  rigor  which  sometimes  follows 
catheterisation  is  probably  also  toxic  in  origin,  since  it  rarely  occurs 
except  when  there  is  a  raw  surface  in  a  urinary  tract  which  is  not 
aseptic.  In  all  these  toxic  rigors,  although  the  shivering  patient 
has  a  sensation  of  cold,  his  t:mperature  meanwhile  is  rising, 
and  it  continues  to  rise  until  the  rigor  stops.  He  has  the  sensa- 
tion of  cold  because  by  vasomotor  action  the  blood  is  driven  out 
of  his  skin,  which  is  therefore  cooled  and  is  actually  cold,  although 
the  temperature  of  the  blood  is  raised. 

88 


INVOLUNTARY    MOVEMENTS  89 

Transient  flickering  or  quivering  of  a  muscle,  a  condition  known 
as  myokymia  (or  more  popularly  as  "  live  flesh  "),  affecting  a  few 
muscle-bundles  of  a  single  muscle,  without  producing  movement 
of  a  joint,  is  not  uncommon  in  people  who  are  anaemic,  neurasthenic, 
or  out  of  health.  It  is  specially  common  in  the  orbicularis  oculi 
and  in  some  of  the  larger  muscles  of  the  limbs,  e.g.  the  deltoid  and 
biceps  in  the  upper  limb,  the  glutei  and  quadriceps  in  the  lower. 
This  variety  of  myokymia  is  not  associated  with  muscular  atrophy, 
nor  with  any  alteration  of  electrical  excitability.  It  is  unaffected 
by  rest  or  by  voluntary  exertion,  and  has  no  serious  significance. 

Sometimes,  however,  fibrillary  movement  occurs  in  organic 
lesions  of  the  lower  motor  neurone.  Thus  in  the  muscular  atrophy 
of  chronic  anterior  poliomyelitis,  of  amyotrophic  lateral  sclerosis,  and 
of  some  cases  of  syringomyelia,  diseases  in  which  the  ceUs  of  the 
anterior  cornua  are  undergoing  slow  degeneration,  there  may  be  seen 
fibrillary  or  fascicular  tremors  in  the  wasting  muscles.  This 
quivering  myokymia  can  often  be  elicited  by  gentle  flicking,  or  by 
a  breath  of  cold  air  blown  over  the  skin.  A  precisely  similar 
fibrillary  tremor  occurs  in  the  wasting  tongue  of  bulbar  paralysis, 
when  the  degenerative  process  has  involved  the  hypoglossal 
nuclei.  Fibrillary  tremor  does  not  occur  in  the  primary 
myopathies,  whether  atrophic  or  pseudo-hypertrophic  in  type. 
In  other  cases  fibrillary  tremor  occurs  in  the  distribution  of  a 
motor  nerve  which  has  begun  to  recover  from  previous  paralysis. 
It  is  not  uncommon  in  the  face  during  convalescence  from  facial 
palsy,  and  sometimes  it  persists  for  months  and  years  after 
voluntary  power  has  returned,  as  in  the  case  of  a  professional 
fi'iend  of  my  own  who  is  otherwise  perfectly  well.  More  usually 
the  myokymia  passes  of!  when  motor  power  has  been  restored. 

Somewhat  diiTerent  in  appearance  is  the  condition  known 
as  myoclonus,  a  rare  disease,  characterised  by  paroxysms  of 
sudden  shock-like  contractions  in  various  muscles,  lasting  for 
several  minutes  at  a  time,  irregular  in  rhythm  and  varying  in 
rapidity  from  ten  to  fifty  per  minute.  In  slight  cases  the  twitches 
may  be  insufficient  to  produce  movements  in  the  affected  parts. 
The  muscles  affected  are  usually  those  of  the  limbs,  especially  the 
lower  limbs,  often  symmetrically  on  the  two  sides,  but  contractions 
may  also  occur  in  the  trunk  and  even  in  the  face.  Sometimes  the 
diaphragm  and  the  larynx  are  affected,  so  that  curious  grunting 
respiratory  sounds  are  produced.     There  is  no  muscular  atrophy 


90 


NERVOUS    DISEASES 


or  alteration  in  electrical  excitability.  The  spasms  cease  during 
sleep.  Several  varieties  of  myoclonus  have  been  observed ;  in 
one — Friedreich's  'paramyoclonus  multiflex,  usually  a  disease  of 
adult  life  —  the  myoclonus  ceases  on  voluntary  movement. 
Another  variety  is  Unverricht's   family  myoclonus  or  myoclonus 


Fig.  41. — Unverricht's  family  myoclonus  or  "  mj^oclonus  epilepticus  "  in  a  boy 
aged  13.  Besides  the  muscles  indicated  by  shading  in  the  diagram,  the  soft 
palate  was  also  affected. 


epilepticus,  in  which  several  members  of  a  family  are  affected,  all 
belonging  to  the  same  generation,  though  the  disease  is  not  handed 
down  from  parent  to  child.  In  addition  to  the  myoclonus,  these 
patients  have  epileptiform  fits,  and  they  tend  ultimately  to  become 
more  or  less  demented.  Moreover,  the  muscular  contractions  in 
family  myoclonus  are  intensified  by  voluntary  movement  and  by 
psychical  excitement.     Family  myoclonus  usually  manifests  itself 


INVOLUNTARY    MOVEMENTS 


91 


in  early  life,  often  at  or  before  puberty.  Thus  in  a  little  boy  of 
thirteen  suffering  from  myoclonus  affecting  the  muscles  of  the  neck, 
shoulders,  trunk,  thighs  and  cremasters  (see  Fig.  41),  the  condition 
had  existed  since  the  age  of  four,  and  he  had  also  epileptiform 
fits.  Two  elder  brothers  were  similarly  affected,  both  of  whom, 
as  the  patient  graphically  put  it,  began  to  "  chck  "  at  the  age 


Fig.  42. — Friedreich's  paramyoclonus  multiplex  in  a  man  aged  50  (the  affected 
muscles  are  indicated  by  shading). 


of  seven.  On  the  other  hand,  another  patient  suffering  from 
Friedreich's  paramyoclonus  showed  no  symptoms  of  the  disease 
till  the  age  of  forty-seven.  He  never  had  fits,  and  at  the  age  of 
fifty,  when  he  came  under  observation,  he  had  myoclonic  shocks 
limited  to  the  muscles  indicated  in  the  accompanying  diagram 
(Fig.  42).  Another  variety  is  the  nystagmus-myoclonus  of  Lenoble 
and  Aubineau,  to  which  we  shall  refer  later  (see  p.  144). 


92  NERVOUS    DISEASES 

We  next  pass  to  the  consideration  of  tremors.  The  term  "  tremor" 
is  appUed  to  involuntary  rhythmic  oscillations  of  one  or  more  parts 
of  the  body,  resulting  from  the  alternate  contraction  of  muscle - 
groups  and  of  their  antagonists.  A  simple  tremor  is  one  which 
afiects  a  single  muscle-group  and  its  antagonists,  whilst  in  a  com- 
found  tremor  several  groups  with  their  antagonists  are  in  action, 
producing  a  complex  movement,  e.g.  flexion  and  extension  of  the 
fingers  combined  with  pronation  and  supination  of  the  forearm. 
Tremors  may  be  rapid  or  slow  ;  they  may  be  diminished  or  increased 
by  voluntary  exertion,  and  they  generally  cease  during  sleep. 

We  must  not  forget  that  an  ordinary  voluntary  muscular 
movement  is  not  the  result  of  a  continuous  muscular  contraction, 
but  is  constituted  by  the  fusion  of  a  rapid  succession  of  short  single 
contractions,  averaging  from  ten  to  twelve  per  second.  In  condi- 
tions of  temporary  fatigue  or  of  chronic  asthenia  the  rate  of  these 
muscle  discharges  becomes  slower  and  less  regular,  so  that  the 
individual  muscular  contractions  fuse  less  perfectly  and  the  result 
is  a  very  fine  tremor.  In  emotional  excitement — more  often  in 
states  of  fear  than  from  pleasurable  emotion — there  may  be  a  fine 
rhythmic  tremor  of  about  eight  or  nine  oscillations  per  second, 
famihar  to  the  knees  of  many  a  public  speaker.  The  same  occurs 
in  exophthalmic  goitre.  This  tremor  is  made  more  apparent  by 
voluntary  exertion.  It  is  best  elicited  by  making  the  patient  hold 
his  hands  horizontally  in  front  of  him,  with  the  fingers  widely 
spread.  We  can  then  feel  the  tremor  even  better  than  see  it,  by 
placing  our  own  fingers  lightly  on  the  dorsum  of  the  patient's  hand. 
This  fine  tremor  afiects  all  the  limbs,  and  in  many  cases  can  be 
detected  by  simply  placing  one's  hand  on  the  patient's  shoulder. 
Tremulous  respiration,  in  which  the  tremor  is  synchronous  with  that 
of  the  outstretched  hands,  is  also  one  of  the  most  constant  signs  of 
exophthalmic  goitre.     It  is  best  marked  during  full  expiration.^ 

Similar  fine  tremors  also  occur  in  certain  toxic  conditions.  The 
tremor  of  chronic  alcoholic  poisoning  is  familiar  to  the  lay  observer, 
and  when  an  alcoholic  patient  becomes  delirious  and  maniacal 
(usually  following  a  sudden  enforced  abstinence),  his  tremors  are 
so  evident  that  the  condition  is  termed  "  delirium  tremens."  But 
other  poisons  besides  alcohol  produce  fine  tremors  :  for  example, 
nicotine  poisoning  from  excessive  cigarette-smoking,  also  chronic 
poisoning  by  lead,  mercury,  chloral,  cocaine,  tea,  coffee,  tobacco,  &c. 

^  Minor,  Zeitschrift  f.  d.  ges.  Neurologie  u.  Psychiatrie,  1912,  Bd.  12. 


INVOLUNTARY    MOVEMENTS 


93 


In  cases  of  suspected  alcoholism  a  valuable  corroborative  sign, 
known  as  Quinquaud' s  fingrr-cre'pitation,  may  often  be  elicited.  In 
testing  for  this,  we  make  the  patient  extend  the  fingers  at  the  inter- 
phalangeal  joints  and  press  them  at  right  angles  to  the  palm  of  our 
own  hand,  which  we  hold  in  a  vertical  position.  For  the  first  two 
or  three  seconds  nothing  particular  is  noticed,  but  if  the  patient 
be  a  chronic  alcoholic,  we  soon  begin   to   feel  a  series   of  slight 


Fig.  43. — Paralysis  Agitans, 
left-sided. 


Fig.  44. — Paralysis  Agitans: — 
the  same  patient  as  in  Fig .43, 
three  years  later. 


shocks,   as   if   the  phalanges  of  each   finger  were   knocking,   one 
against  the  other,  trying  to  reach  our  palm. 

The  tremor  of  paralysis  agitans  occurs  at  rest  and  is  generally 
rather  coarse,  varying  in  different  cases  from  four  to  seven  oscilla- 
tions per  second.  It  produces  joint  movements,  e.g.  the  well-known 
"  pill-rolling  "  movement  of  the  thumb  and  fingers,  flexion-extension 
movement  of  the  wrists,  pronation- supination  of  the  forearm,  flexion- 
extension  of  the  ankle,  &c.  The  coarser  the  movement,  the  slower 
is  the  rhythm.     Paralysis  agitans  generally  begins  unilaterally,  and 


94  NERVOUS    DISEASES 

may  remain  confined  to  one  side  for  some  time  before  ultimately  be- 
coming bilateral,  as  may  be  seen  in  Figs.  43  and  44,  which  are  taken 
from  the  same  patient  at  an  interval  of  three  years.  Usually  the 
tremor  of  paralysis  agitans  can  be  temporarily  controlled  by 
voluntary  exertion.  But  this  is  not  always  so  ;  indeed,  cases  occur  in 
which  voluntary  movement  increases  the  tremor.  Paralysis  agitans 
is  always  accompanied  by  rigidity  in  the  afltected  muscles ;  in 
fact,  rigidity  may  be  well  marked  without  tremor,  in  the  so-called 
"  paralysis  agitans  sine  agitatione."  An  attack  of  ordinary 
hemiplegia  occurring  in  a  patient  with  paralysis  agitans  arrests 
the  tremor  in  the  hemiplegic  limbs,  but  if  the  hemiplegia  clears 
up,  the  tremor  may  subsequently  reappear. 

Senile  tremor  is  not  unlike  the  tremor  of  paralysis  agitans, 
but  its  onset  occurs  much  later  in  life.  Moreover,  it  begins 
bilaterally,  especially  in  the  head,  jaw,  and  lips,  and  is  unaccom- 
panied by  the  characteristic  rigidity  of  Parkinson's  disease. 
Thus  in  a  famous  old  admiral  it  began  at  the  age  of  eighty-four 
as  a  gentle  antero-posterior  tremor  of  the  tongue,  with  a  syn- 
chronous movement  of  the  orbicularis  oris.  Both  his  hands  had 
tremor  and  an  interosseal  attitude  like  that  of  paralysis  agitans, 
but  without  rigidity. 

In  rickety  children,  especially  during  the  second  six  months 
after  birth,  we  sometimes  observe  a  peculiar  involuntary  rotatory 
or  nodding  tremor  of  the  head  which  usually  comes  on  quite 
suddenly  in  winter-time  and  is  known  as  spasmus  nutans.  It 
is  generally  accompanied  by  fine,  rapid  nystagmus,  either  hori- 
zontal, vertical  or  rotatory,  which  may  be  more  marked  in  one 
eye  than  in  the  other.  If  we  fix  the  child's  head,  the  nystagmus 
increases.  The  head  movement  is  more  often  a  lateral  rotation 
than  an  antero-posterior  nodding.  It  stops  when  the  child's  eyes 
are  closed,  either  voluntarily  or  artificially.  The  symptom 
persists  for  six  or  eight  weeks  or  longer,  and  then  passes  off, 
perhaps  to  return  again  in  the  following  winter.  It  is  not 
associated  with  any  mental  defect. 

Head-rolling  is  another  variety  of  involuntary  rhythmic  move- 
ment met  with  in  children,  chiefly  below  the  age  of  two  years. 
Many  of  the  patients  are  rickety  and  a  large  proportion  have  otitis 
media,  latent  or  evident.-^  The  movement  is  more  vigorous  than 
that    of    spasmus  nutans,    it    is    unassociated    with    nystagmus, 

^   Still,  Clinical  Journal,  Nov.  28,  1906. 


INVOLUNTARY    MOVEMENTS  95 

and  it  ceases  when  the  child  sits  up,  only  occurring  when  he 
lies  down. 

Rhythmic  tremor  sometimes  occurs  in  gross  brain  disease. 
Thus,  for  example,  in  cases  of  lesions  in  the  tegmental  region 
of  the  pons  or  crus  cerebri,^  affecting  the  rubrospinal  tract 
(which  descends  from  the  red  nucleus  into  the  lateral  column  of 
the  opposite  side),  or  in  lesions  of  the  lenticular  nucleus,  we 
occasionally  observe  a  slow  rhythmic  tremor  of  the  limbs  of 
the  opposite  side,  chiefly  in  the  hand  and  foot.  This  tremor  is 
increased  by  excitement  or  voluntary  movement,  but  ceases  during 
sleep.  In  the  diagnosis  of  such  cases  we  have,  besides  the  tremor, 
the  other  localising  signs  of  a  gross  destructive  lesion.  Thus  if 
the  ocular  nuclei  (which  lie  dorsal  to  the  red  nucleus)  be  affected, 
there  is  ocular  palsy  of  the  nuclear  type ;  if  the  pyramidal  tract 
be  affected  there  is  spastic  hemiplegia ;  and  if  the  sensory  tract, 
traversing  the  internal  capsule  and  optic  thalamus,  be  implicated, 
we  have  hemianaesthesia.  When  a  unilateral  lesion  of  one  crus 
cerebri  produces  oculomotor  paralysis  of  one  side  with  tremor  of 
the  opposite  arm  and  leg,  this  is  known  as  Benedikfs  syndrome. 
Moreover,  certain  lesions  of  the  optic  thalamus  cause  loss  of  emo- 
tional mobility  in  the  opposite  side  of  the  face  in  laughing  or 
crying,  with  little  or  no  weakness  on  voluntary  movement. 

Progressive  lenticular  degeneration,  associated  with  cirrhosis  of 
the  Hver,  is  a  rare  family  extra-pyramidal  disease  which  occurs 
in  young  people."  It  is  invariably  progressive  and  fatal,  usually 
within  two  to  seven  years.  It  is  recognised  by  the  presence  of 
bilateral  rhythmic  tremors  of  the  hmbs,  increased  on  voluntary 
movement,  together  with  marked  hyper-tonicity  of  the  limbs  and 
face,  the  face  being  "  set  "  in  a  spastic  smile.  Nevertheless,  inas- 
much as  the  disease  leaves  the  pyramidal  paths  unaffected,  there  is  no 
true  motor  paralysis,  although  voluntary  movements  are  interfered 
with  by  the  muscular  rigidity.  There  is  dysphagia  and  dysarthria, 
and  a  degree  of  emotionalism,  the  spastic  smile  tending,  on  slight 
provocation,  to  become  a  spasmodic  laugh.  The  optic  discs,  pupils, 
and  cranial  nerves  are  normal.  There  is  no  nystagmus.  There 
are  no  sensory  abnormalities.  The  deep  reflexes  are  normal.  The 
plantar  reflexes  are  flexor  in  type  and  the  abdominal  reflexes  are 
preserved.     Post-mortem  both  lenticular  nuclei  are  found  to  be 

1  Holmes,  Brain,  1904,  vol.  xxvii.  p.  327. 

2  Wilson,  ibid.,  1911,  p.  295. 


96  NERVOUS   DISEASES 

degenerated,  and  in  advanced  cases  there  may  be  a  cavity  in  each 
corpus  striatum.  The  brain  and  spinal  cord  are  otherwise  normal. 
The  liver  shows  intense  multilobular  "  hob-nail "  cirrhosis. 

In  some  cases  of  tumour  of  the  frontal  lobe,  there  is  a  fine 
tremor  in  the  upper  limb  when  it  is  held  horizontally  forwards. 
The  tremor  in  such  cases  affects  the  ipso-lateral  limb  ;  thus  in  a 
right-sided  frontal  tumour  we  may  find  tremor  in  the  right  hand. 

Let  us  now  pass  to  the  irregular,  non-rhythmic,  spontaneous 
movements.  Of  these,  ordinary  "rheumatic"  chorea  furnishes 
one  of  the  most  striking  examples.  All  are  familiar  with  the 
irregular,  jerking,  wriggling,  grimacing  movements  of  a  choreic 
child.  They  may  affect  the  face,  soft  palate,  tongue,  trunk,  limbs, 
and  even  the  muscles  of  respiration.  The  movements  of  the 
limbs  are  often  more  marked  on  one  side  than  on  the  other,  and 
may  be  confined  to  one  side — so-called  hemi-chorea.  Choreic  move- 
ments occur  spontaneously  but  are  increased  by  emotion  or  by 
voluntary  movements.  They  cease  during  sleep.  The  muscles 
of  choreic  limbs  have  a  diminished  tonus  (hypotonia).  A  good 
method  of  eliciting  choreic  movements  in  a  slight  case  of  the 
disease,  is  to  make  the  child  hold  both  hands  above  the  head, 
when  after  a  few  seconds  slight  involuntary  movements  appear  in 
the  fingers  of  one  or  both  sides. 

Huntington's  chorea  is  a  hereditary  variety  of  chorea  which 
comes  on  after  middle  life  and  becomes  steadily  worse.  It  is  asso- 
ciated with  progressive  dementia. 

Hyoscine  chorea,  whose  symptoms  are  similar  to  those  of  ordi- 
nary chorea,  occurs  during  acute  intoxication  with  hyoscine,  and 
is  sometimes,  but  not  invariably,  associated  with  mild  delusions. 

The  movements  of  athetosis  or  "  mobile  spasm  "  are  different, 
occurring  as  they  do  most  commonly  in  the  spastic  limbs  of  old- 
standing  hemiplegics  (chiefly  after  infantile  hemiplegia).  Athetosis 
never  occurs  in  a  limb  which  is  completely  paralysed,  but  only  when 
some  degree  of  voluntary  power  survives.  The  movements  are 
usually  confined  to  the  upper  limb,  and  consist  of  very  slow,  irregular, 
twisting  movements,  most  marked  in  the  fingers  and  wrist,  but  in 
severe  cases  affecting  the  forearm,  elbow,  shoulder,  and  even  the  lower 
limb,  where  the  most  common  involuntary  movement  is  a  hyper- 
extension  of  the  great  toe.  Only  in  bilateral  athetosis  (generally, 
though  not  always,  following  diplegia)  do  the  movements  affect  the 
face,  causing  hideous  grimacing  (see  Fig.  54,  p.  124).     In  a  typical 


INVOLUNTARY    MOVEMENTS  97 

case  the  hand  movements  consist  of  slow  flexion,  then  hyper-exten- 
sion and  spreading  out  of  the  fingers,  irregularly,  one  after  another. 
Combined  with  this,  there  is  alternate  abduction  and  opposition 
of  the  thumb,  with  flexion  or  extension  of  the  wrist,  and  prona- 
tion or  supination  of  the  forearm.  Fig.  45  is  taken  from  a  well- 
marked  case  of  athetosis  in  which  the  movements  affected  all  the 


Fig.  45. — ^  Athetosis  in  a  woman  aged  29,  the  subject  of  right-sided  hemi- 
plegia of  nineteen  years'  duration.  There  was  severe  paralysis  of  the 
right  upper  limb  from  the  shoulder  downwards.  The  figures  show  athetosis 
of  fingers,  wrist,  and  elbow. 

joints  of  the  upper  limb.  Athetosis  is  intensified; by  voluntary 
movement  whether  of  the  paralysed  limb  or  of  the  opposite 
unafltected  hand.  It  cannot  be  controlled  by  voluntary  effort, 
and  sometimes  persists  even  during  sleep. 

Spontaneous  "  associated  movements "  occur  involuntarily  in 
many  cases  of  hemiplegia.  Thus  the  patient,  when  attempting  to 
draw  up  the  hemiplegic  leg,  involuntarily  dorsiflexes  the  ankle 
and  hyper-extends  the  hallux,  or  when  flexing  the  fingers,  he  in- 
voluntarily dorsiflexes  the  wrist,  and  so  on.     (See  later,  p.  223.) 

In  certain  cases  of  hemiplegia  and  diplegia,  involuntary  move- 

G 


98  NERVOUS  DISEASES 

ments  of  the  limbs,  especially  of  the  upper  limbs,  can  be  produced 
by  changing  the  posture  of  the  head,  whether  actively  or  passively. ^ 
These  conjugate  automatic  movements  are  analogous  to  those 
observed  experimentally  in  decerebrate  animals.^  In  such  animals, 
with  "  decerebrate  rigidity "  and  an  extended  posture  of  the 
limbs,  there  occurs  an  exaggeration  of  the  extension  of  the  limb 
towards  which  the  animal's  face  is  turned  (facial  limb)  together 
with  a  diminution  of  the  extension  of  the  limb  towards  which  the 
occiput  is  turned  (occipital  limb).  Similarly  in  certain  cases  of 
diplegia,  if  the  patient's  head  be  turned  to  the  right,  we  observe 
that  the  left  upper  limb  slowly  becomes  tonically  flexed,  whilst 
the  right  becomes  extended.  The  phenomenon  takes  about 
a  minute  to  reach  its  maximum.  If  we  now  turn  the  head 
to  the  opposite  side,  the  attitude  of  the  upper  limbs  becomes 
reversed.  Similar  phenomena  are  sometimes  seen  in  hemiplegia, 
being  limited,  of  course,  to  the  hemiplegic  limbs.  Thus  we 
may  observe  flexion  of  the  hemiplegic  upper  limb  when  the  face  is 
turned  away  from  the  hemiplegic  side,  and  extension  of  the  hemi- 
plegic limb  when  the  face  is  turned  towards  the  hemiplegic  side. 

Many  healthy  people  make  automatic  extension  movements  of 
the  upper  limbs  during  the  act  of  yawning.  By  the  ancients 
these  were  termed  pandiculation.  Such  movements  are  often 
well  seen  in  the  paralysed  limbs  of  a  case  of  severe  hemiplegia 
when  the  patient  yawns  or  is  tickled,  and  the  patient  may  harbour 
vain  hopes  of  a  return  of  motor  power  by  observing  extension 
movements  of  his  paralysed  fingers  or  elevation  of  the  paralysed 
arm.  Unfortunately  these  movements  are  not  a  hopeful  sign  in 
hemiplegia ;  on  the  contrary,  the  more  severe  the  lesion  of  the 
pyramidal  tract,  the  more  marked  is  the  pandiculation.  It 
does  not  occur  in  limbs  which  are  the  subjects  of  athetosis 
or  other  involuntary  movements.  Pandiculation  has  been  as- 
cribed by  Bertolotti  ^  to  irritation  of  the  thalamic  centres. 

It  is  not  uncommon,  in  cases  of  chronic  hemiplegia,  to  observe 
involuntary  synkinetic  movements  of  the  opposite  non-paralysed 
limb  during  powerful  voluntary  effort  to  move  the  paralysed  limb. 
The  converse  condition  also  occurs,  in  which  synkinetic  movement 
of  the  paralysed  limb   occurs  when  the  opposite  non-paralysed 

1  Marie  and  Foix,  Revue  neurologique,  1914,  p.  120. 
^  Magnus,  Munch,  nied.  Wochenschrift,  1912,  No.  13. 
^  Revue  neurologique,  1905,  p.  953. 


INVOLUNTARY    MOVEMENTS 


99 


limb  is  powerfully  innervated.  Thus  when  a  hemiplegic  patient 
grasps  strongly  or  stretches  out  his  fingers  powerfully  with  the 
non-paralysed  hand,  the  hemiplegic  fist  may  be  correspondingly 
clenched  or  opened.  Sometimes  even  passive  movements  of  one 
hand  may  be  executed  bilaterally.  A  degree  of  bimanual  synkinesia 
may  be  physiological,  especially  in  children,  so  that  movements 
tend  to  be  carried  out  bilate- 
rally. Occasionally  this  con- 
dition persists  into  adult  life. 
It  may  run  in  families,  when 
it  is  usually  to  be  regarded 
as  a  stigma  of  a  neuropathic 
inheritance. 

Spontaneous  movements 
also  occur  in  cases  of  advanced 
Friedreich's  ataxia,  being  most 
marked  in  the  head,  neck,  and 
face.  They  commonly  consist 
in  irregular  nodding  move- 
ments of  the  head  or  grimac- 
ing, which  has  been  called 
"  nystagmus  of  the  face." 
But  in  Friedreich's  ataxia  the 
most  outstanding  feature  is 
inco-ordination  of  voluntary 
movements.  The  absence  of  the  knee-jerks,  the  deformity  of  the 
feet,  the  scoliosis,  &c.,  will  all  point  to  a  correct  diagnosis. 

Spontaneous  movements,  pseudo-athetosis,  also  occur  in  certain 
cases  of  talies  in  which  there  is  severe  impairment  of  joint-sense 
and  ataxia  of  the  muscular  tonus.  The  movements  are  chiefly  seen 
in  the  fingers  and  wrists,  and  can  best  be  demonstrated  by  making 
the  patient  close  his  eyes  and  hold  his  hands  steadily  in  the  air 
with  the  fingers  extended.  In  a  few  seconds  we  observe  slow 
irregular  -flexion  or  extension  movements  of  the  fingers,  which 
gradually  assume  curiously  distorted  attitudes,  of  which  the  patient 
is  totally  unaware.  (See  Pig.  46,  also  Fig.  163,  p.  323,  where  similar 
movements  have  occurred  in  the  lower  Hmbs.) 

Again,  in  general  paralysis  of  the  insane,  spontaneous  tremors 
of  an  irregular  type  are  frequently  observed,  even  when  the  patient 
is  at  rest.     They  occur  chiefly  in  the  face,  especially  if  the  patient 


Fig.  46. — Tabetic  pseudo-athetosis  on 
closing  the  eves. 


100  NERVOUS    DISEASES 

be  emotionally  excited  or  just  about  to  speak.  Waves  of  fibrillary 
tremor  appear,  rippling  along  the  muscles  of  the  lips,  tongue,  and 
face.  Irregular  tremors  of  an  intentional  type  are  also  frequently 
present,  especially  in  the  upper  limbs.  Their  rhythm  varies  from 
5  to  9  per  second.  They  can  often  be  demonstrated  by  asking  the 
patient  to  write.  Here  we  have  other  physical  signs  to  guide  us, 
e.g.  the  slurring  articulation,  the  irregular  or  unequal  pupils,  fre- 
quently of  Argyll-Robertson  type,  exaggeration  or  loss  of  the 
knee-jerks,  the  condition  of  the  cerebro-spinal  fluid,  and  the  char- 
acteristic mental  symptoms. 

There  is  another  great  group  of  involuntary  movements  which 
includes  the  habit  spasms,  the  tics,  and  the  reflex  spasms.  A 
proper  classification  of  these  is  well-nigh  impossible,  since  the 
different  varieties  merge  into  each  other.  All  are  most  common 
in  people  of  "  nervous "  constitution,  all  are  increased  by 
emotion,  and  they  cease  during  sleep.  Slight  degrees  of  habit- 
spasm  may  occur  without  any  other  sign  of  functional  disease. 
Public  speakers,  such  as  clergymen,  barristers,  actors,  and  even 
medical  lecturers,  occasionally  have  little  unconscious  "  tricks " 
of  movement.  A  distinguished  university  professor  has  frequent 
clonic  jerks  of  the  frontales  muscles,  which  suddenly  elevate  his 
eyebrows  ;  a  popular  comedian  makes  rapid  blinking  movements 
of  both  eyes  (blepharo-spasm)  when  he  advances  towards  the 
foot-lights ;  a  young  lady  has  clonic  spasms  of  both  platysmata 
when  her  neck  is  exposed  in  evening  dress  at  dinner  parties,  and 
so  on.  Such  minor  degrees  of  habit-spasm  are  usually  bilateral 
and  occur  without  any  local  exciting  cause. 

More  severe  varieties  of  habit -spasm  are  included  under  the 
term  "Tic."  A  tic  is  of  cortical,  not  reflex  origin,  and  consists 
in  the  frequent  explosive  repetition  of  the  same  motor  act — gener- 
ally a  violent,  irregular  one,  such  as  rapid  shaking  or  tossing  of 
the  head,  grimacing,  wriggling  of  the  shoulder,  &c.  It  passes  off 
as  suddenly  as  it  comes  on.  Moreover,  it  does  not  interfere  with 
voluntary  movements.  For  example,  however  violent  a  tic  of  the 
right  shoulder  or  arm  may  be,  the  patient's  handwriting  shows 
no  abnormality.  As  Patrick  ^  has  put  it,  when  the  impulse  to  tic 
can  no  longer  be  controlled,  the  patient  takes  pen  from  paper, 
executes  his  tic  and  then  resumes  writing.  At  first  sight,  tic  might 
be  confounded  with  chorea.     But  chorea  does  not  repeat  the  same 

1  Journal  of  American  Med.  Assoc,  Feb.  21,  1905. 


INVOLUNTARY   MOVEMENTS 


101 


movement  regularly  again  and  again.  Patients  who  have  severe 
tic  usually  show  signs  of  mental  degeneracy.  This  does  not 
mean  that  they  are  necessarily  dejficient  in  intelligence.  On  the 
contrary,  they  are  often  "  superior  degenerates,"  bright  and 
lively,  but  mentally  immature,  capricioas,  emotional,  psychas- 
thenic, and  frequently  the  subjects  of  obsessions  and  various 
forms  of  "  phobia."  The  greater 
the  psychical  abnormality,  the 
more  inveterate  is  the  tic. 
"  Tiqueurs  "  often  have  other 
evidences  of  the  psychasthenic 
constitution,  such  as  explosive 
articulation,  "  word-swallowing," 
sudden  stoppage  of  speech,  dis- 
ordered respiration,  echolalia  (re- 
petition of  a  particular  word  or 
phrase),  or  coprolalia  (repetition  of 
a  blasphemous  or  obscene  word). 

Spasmodic  torticollis  is  one  of 
the  commonest  and  most  severe 
varieties  of  tic.  Though  the  result 
of  the  movement  is  to  jerk  the 
head  to  one  side,  commonly  to 
the  left  (see  Fig.  47),  the  spasm  is 
really  a  bilateral  affair,  since  muscles  on  both  sides  of  the  neck, 
protagonists  and  antagonists,  are  employed  to  produce  the  move- 
ment. It  is  sometimes  combined  with  a  backward  jerk,  a  so- 
called  retro-collic  spasm.  The  movement  may  be  tonic,  clonic,  or 
a  combination  of  the  two — tonico-clonic.  The  patient  can  often 
curb  the  movement  by  means  of  some  antagonistic  gesture  of  his 
own  invention,  e.g.  by  light  pressure  on  the  chin  with  his  finger. 
Severe  torticolHs  usually  begins  after  middle  life.  At  first  occurring 
in  paroxysms,  it  ultimately  becomes  continuous  during  waking  hours, 
and  the  affected  muscles  become  hypertrophied  from  over-use. 

Besides  idiopathic  spasmodic  torticollis,  which  comes  on  ap- 
parently spontaneously,  certain  cases  have  a  definite  exciting 
cause  and  should  be  classed,  not  with  the  tics,  but  with  the  reflex 
spasms  which  we  shall  consider  presently.  Thus,  for  example, 
we  may  have  neuralgic  torticollis,^  in  which  an  occipital  neuralgia 

1  Cruchet,  Traite  des  Torlicolis  Spasmodiques,  Paris,  1907. 


Fig.  47. — Spasmodic  torticollis,  with 
secondary  hypertrophy  of  right 
sterno-mastoid. 


102  NERVOUS    DISEASES 

or  a  painful  tooth  is  followed  by  spasmodic  torticollis,  usually  tonic 
in  form.  When  the  neuralgia  passes  off,  the  muscular  spasm  ceases 
also.  Again,  we  may  have  labyrinthine  torticollis,^  due  to  chronic 
irritation  of  one  of  the  semicircular  canals.  In  such  cases  the 
torticollic  spasm  has  the  object  of  mitigating  vertigo,  which  would 
occur  if  the  head  were  not  kept  leaning  over  to  the  opposite  side. 
A  torticollis  thus  initiated  may  become  inveterate,  but  some  cases 
are  cured  by  the  administration  of  quinine.  A  small  proportion 
of  cases  are  examples  of  professional  torticollis,  occurring  only  at 
the  moment  of  performing  a  special  act,  especially  in  cobblers  and 
tailors,  who  have  to  turn  the  head  and  eyes  to  follow  the  needle. 
Such  cases  are  more  properly  to  be  classed  with  the  occupation- 
neuroses  (see  p.  265).  Spasmus  nutans,  head-rolling,  and  other 
rhythmic  movements  (see  p.  94),  must  not  be  confounded  with 
true  torticollis,  in  which  the  spasms  are  either  tonic  or  irregularly 
clonic. 

There  is  another  group  of  movements  which,  originally  excited 
by  some  peripheral  irritation,  are  classed  as  reflex  spasms.  A 
spasm,  unlike  a  tic,  begins  locally,  perhaps  in  a  single  muscle, 
and  spreads  to  adjacent  muscles.  When  the  exciting  stimulus 
is  unilateral,  the  reflex  spasm  is  usually  unilateral  also,  but 
not  invariably  so,  for  bilateral  reflex  spasms  also  occur,  as  in 
tonic  and  clonic  contraction  of  the  orbiculares  oculorum  (ble- 
pharospasm), the  result  of  corneal  or  conjunctival  inflammation, 
or  as  in  the  case  where  a  vaginal  caruncle  or  anal  fissure 
produces  vaginismus  with  bilateral  adductor  spasm.  Of  the 
unilateral  reflex  spasms  one  of  the  most  striking  is  the  intense 
facial  spasm  which  occurs  in  severe  cases  of  trigeminal  neuralgia  or 
tic  douloureux,  which  is  not  a  true  tic  but  a  reflex  spasm.  In 
this  disease  the  patient  has  paroxysms  of  agonising  pain  in  one  or 
more  divisions  of  the  trigeminal  nerve.  During  a  paroxysm,  the 
face  on  the  side  of  the  pain  is  thrown  into  strong  tonic  con- 
traction, the  eye  is  closed,  the  mouth  is  drawn  up  on  the  affected 
side,  and  the  patient  often  presses  his  hand  desperately  over 
the  site  of  pain.  Only  when  the  acute  stage  of  the  paroxysm 
passes  off  do  the  facial  muscles  relax. 

Less  severe  paroxysmal  facial  hemi-spasm,  either  tonic  or  clonic, 
usually  commencing  with  waves  of  flickering  fibrillary  movement, 
especially  in  the  orbicularis  oculi,  closely  resembling  the  move- 

^  Curschmann,  Deutsche  Zeitschrift  fiir  Nervenheilkunde,  1907,  p.  305. 


INVOLUNTARY    MOVEMENTS 


103 


merits  produced  by  faradic  stimulation  and  implicating  some  or 
all  of  the  facial  muscles,  may  arise  from  other  reflex  causes, 
generally  in  the  territory  of  the  fifth  nerve,  such  as  a  decayed 
tooth,  a  non-erupted  wisdom-tooth,  a  nasal  polypus,  &c.  Facial 
hemi-spasm,  unUke  tic 
douloureux,  is  painless. 
Occasionally  it  occurs 
primarily,  without  ap- 
parent cause,  as  in  the 
patient  shown  in  Fig.  48. 
It  also  occurs,  less  fre- 
quently, in  lesions  of  the 
facial  nerve  itself,  as,  for 
example,  when  tumours 
or  abscesses  compress  the 
nerve.  Sometimes  it  fol- 
lows an  attack  of  ordinary 
facial  palsy,  less  com- 
monly it  may  precede  its 
onset,  so  that  in  every  case 
of  facial  hemi-spasm  we 
should  search  for  local 
lesions  in  the  territory 
not  only  of  the  trigeminal 
but  also  of  the  facial  nerve. 

Sometimes  a  reflex  spasm  may  persist  as  a  habit-spasm,  long 
after  the  original  exciting  cause  has  passed  away.  Such  cases 
can  usually  be  diagnosed  by  their  history.  For  example,  a  lad 
lost  his  left  arm  by  avulsion  in  a  machinery  accident.  The  stump 
was  amputated  at  the  shoulder- joint,  but  clonic  spasms  appeared 
in  the  trapezius  and  scapular  muscles,  and  these  persisted  after 
all  the  posterior  nerve-roots  in  that  region  were  divided  by 
operation.  Certain  well-marked  types  of  blepharospasm  sometimes 
follow  shell-explosions  in  war.  In  one  variety  the  retinae,  owing 
to  the  intense  flash  of  the  bursting  shell,  are  over-stimulated  and 
become  hypersesthetic.  The  patient  endeavours  to  protect  them 
from  light  by  a  vigorous  blepharospasm,  which  may  be  bilateral, 
or,  more  commonly,  unilateral.  In  other  cases,  again,  particles  of 
dust  are  driven  into  the  conjunctivae  by  a  missile  landing  close  in 
front,  and  here  also  a  reflex  blepharospasm  results,  as  in  the  patient 
shown  in  Fig.  48a,  who  was  struck  by  a  fragment  of  bomb  in  the 


Fig.  48. — Left-sided  facial  hemi-spasm. 


104 


NERVOUS    DISEASES 


right  frontal  region,  producing  only  a  superficial  abrasion.  The 
right  eye,  however,  was  bHnd  for  five  days,  and  subsequently  re- 
mained closed  for  over  a  month  by  spasm  of  the  orbicularis,  the 
right  eyebrow  standing  at  a  lower  level  than  the  left.  On 
forcibly  opening  the  lids,  there  was  acute  photophobia,  accom- 
panied by  spasmodic  contrac- 
tion of  the  orbicularis.  The 
pupil  was  slightly  larger  than 
on  the  left  side,  but  reacted 
normally  to  light,  whilst  the 
external  ocular  movements  were 
normal. 

In  any  variety  of  blepharo- 
spasm, if  we  forcibly  open  the 
lids,  the  vision  is  usually  found 
to  be  little  affected,  but  photo- 
phobia is  usually  intense.  The 
blepharospasm  may  persist  for 
periods  varying  from  a  few 
hours  to  several  months. 
Fig.  49  shows  a  case  of  ulnar 
spasm  in  a  blacksmith  who 
sustained  a  severe  jar  of  the  left  elbow  when  holding  an  iron 
bar  which  was  being  hammered  by  a  fellow  workman.  The 
muscles  of  the  left  hand  at  once  became  weak.  Five  months 
later,  tonic  spasm  gradually  set  in,  limited  to  the  intrinsic 
muscles  of  the  hand  suppHed  by  the  ulnar  nerve.  From  con- 
traction of  the  interossei  the  fingers  were  tightly  adducted, 
whilst  the  hypothenar  muscles  produced  opposition  of  the  Little 
finger.  When  examined  a  year  after  the  accident,  this  tonic 
spasm  still  persisted,  and  there  was  blunting  of  sensation  to 
cotton-wool  and  pin-pricks  in  the  ulnar  territory  of  the  hand, 
with  loss  of  vibration-sense  in  the  two  ulnar  fingers.  Prolonged 
massage  and  electrical  treatment  to  the  limb  having  failed  to 
produce  improvement,  the  ulnar  nerve  at  the  elbow  was  injected 
with  normal  saline  solution  containing  a  little  cocaine.  The 
spasm  was  promptly  relieved,  and  a  week  later  no  sensory  or 
motor  abnormality  could  be  detected. 

But  other  cases  occur,  even  of  unilateral  spasm,  without  any 
reflex  exciting  cause  or  the  history  of  one,  and  they  are  difficult 
to  classify.     Thus  a  lady  whose  menopause  occurred  at  the  age  of 


Fig.  -iHA. 


INVOLUNTARY  MOVEMENTS  105 

forty-five,  at  the  same  time  also  lost  most  of  her  property  through 
the  failure  of  a  bank.  She  gradually  developed  clonic  spasm  of 
the  left  facial  muscles.  At  first,  this  consisted  merely  in  a  sUght 
flickering  of  -the  lower  lid  for  a  second  or  two,  every  few  days, 
but  the  condition  gradually  increased  in  severity  until,  when  she 
came  under  observation  thirteen  years  later,  the  spasms  affected 
all  the  facial  muscles  on  one  side,  beginning  as  a  flickering  move- 
ment, and  then  becoming  tonic  and  lasting  from  twenty  to  thirty 
seconds  at  a  time,  the  eye  being  closed,  the  eyebrow  elevated,  the 
angle  of  the  mouth  drawn  outwards,  and  the  platysma  thrown 
into  strong  contraction.     In  the  intervals  between  attacks  the  face 


Fig.  49. — Ulnar  spasm. 

was  symmetrical.     Under  treatment  by  bromides  and  galvanism 
this  patient  rapidly  became  better. 

Finally,  there  are  numberless  varieties  of  hysterical  spasms 
apart  from  the  hysterical  "  fits,"  which  have  already  been  dis- 
cussed. We  can  only  refer  to  some  of  the  commoner  types. 
Thus  saltatory  spasm  consists  of  a  series  of  jumping  or  skipping 
movements,  which  occur  whenever  the  patient  assumes  the  erect 
posture.  A  similar  spasm,  less  severe  in  degree,  may  produce 
paroxysms  of  trembling  in  the  legs,  as  in  a  hysterical  girl  of  nineteen 
with  many  other  stigmata  of  hysteria,  in  whom  the  spasms  ceased 
at  once  when  she  lay  down.  All  sorts  of  movement,  however, 
may  occur  in  hysteria,  simulating  almost  any  kind  of  tremor.  For 
instance,  a  hysterical  woman  of  twenty-one  had  constant  movements 
of  the  face,  left  arm,  and  both  legs,  resembling  those  of  athetosis 
but  very  much  faster.  In  her  case  typical  hysterical  contractures 
and  segmental  anaesthesia  of  the  hysterical  type,  together  with  the 
normal  state  of  the  reflexes,  aided  in  the  diagnosis  of  hysteria, 
which  disease  will  be  further  considered  in  a  subsequent  chapter. 


CHAPTER   VII 

APHASIA 

We  exchange  ideas  with  our  fellow-men  chiefly  by  means  of  speech. 
Speech  is  an  arbitrary  code  of  signals,  vocal  or  written.  These 
signals  are  perceived  by  our  auditory  or  visual  centres.  Every 
country  has  its  own  particular  code  or  language,  which  is  learned 
by  each  of  its  inhabitants.  Gestures  and  mimic  movements,  as 
a  means  of  communication,  although  international,  have  a  very 
limited  field  of  usefulness  as  compared  with  speech.  Two  indi- 
viduals, each  ignorant  of  the  other's  language,  can  certainly  com- 
municate with  each  other  after  a  fashion  by  means  of  gestures 
alone,  yet  they  cannot  express  many  ideas  in  this  way,  but 
only  simple  primitive  emotions  such  as  pleasure,  anger,  surprise, 
and  so  on,  or  pantomimic  imitations  of  certain  acts. 

There  are  three  chief  classes  of  cases  in  which  the  functions 
of  articulate  speech  may  be  lost.  Firstly,  there  are  conditions  in 
which  the  patient's  higher  intellectual  functions  are  in  abeyance, 
either  congenitally  as  in  idiots,  or  from  disease  as  in  acquired 
dementia,  coma,  stupor,  or  in  certain  cases  of  hysteria.  Such 
patients  are  speechless,  but  they  are  not  aphasics.  Secondly,  there 
are  the  cases  where  the  higher  intellectual  centres  are  capable 
of  function,  but  the  cortical  speech-centres  which  control  the 
motor  acts  of  speaking  and  writing,  or  the  sensory  processes  of 
recognising  spoken  or  written  words,  are  diseased,  and  yet  the 
patient  has  not  necessarily  any  paralysis  of  the  peripheral  organs  of 
speech,  nor  is  he  necessarily  deaf  or  blind.  To  this  group  the  term 
"  aphasia "  is  applied.  Lastly,  there  are  the  cases  where,  with 
intact  intellectual  functions  and  normal  cortical  speech-centres, 
there  are  defects  in  the  peripheral  organs  of  articulation,  so  that 
tha  patient  is  unable  to  articulate  distinctly — for  example,  cases 
of  cleft  palate,  post-diphtheritic  palsy  of  the  palate,  facial  or  hypo- 
glossal paralysis,  bulbar  paralysis,  and  so  on.  These  are  afiections, 
not  of  speech  proper,  but  of  articulation. 

Aphasia  may  be  defined  as  impairment  or  loss  of  speech  due 

106 


APHASIA 


107 


to  the  loss  of  memory  for  those  signs,  vocal  or  written,  by  means 
of  which  we  exchange  ideas  with  our  fellow-men.  An  aphasic, 
unless  his  higher  intellectual  centres  are  impaired,  usually  pre- 
serves his  powers  of  gesture  and  of  pantomime.  Aphasia  is  due 
to  disease,  organic  or  functional,  of  certain  well-defined  special 
centres  in  or  near  the  cortex  of  the  brain.  These  cortical  centres 
exist  on  both  sides  of  the  brain,  but  ordinarily  in  right-handed 
people  the  speech-centres  on  the  left  side  of  the  brain  are  pre- 
dominant. 

Let  us  consider  the  speech-centres  somewhat  more  in  detail. 
For  the  interchange  of  ideas  two  distinct  processes  are  required — 


Fig.  50. — Diagram  of  left  cerebral  hemisphere,  showing  approximate 
positions  of  the  centres  concerned  in  speech. 
A.    Auditory  word-centre.        )  <,„,,.„.„ 
V.    Visual  word-centre.  ^-seusory. 

Sp.  Vocal  word-centre.  )  \rnfnr 

W.   Motor  centre  for  writing,  j"^"''"'- 

one  sensory,  the  other  motor.  The  sensory  process  includes  the 
hearing  and  understanding  of  spoken  words,  and  also  the  seeing  and 
understanding  of  written  or  printed  letters.  The  memories  of 
words  heard  and  seen  are  stored  up  in  specialised  parts  of  the 
auditory  and  Adsual  centres,  named  respectively  the  auditory 
word-centre  and  the  visual  word-centre  (Fig.  50).  The  auditory 
word-centre  is  at  the  upper  or  Sylvian  surface  of  the  temporal 
lobe  (anterior  transverse  gyrus  of  Heschl,  Flechsig's  "  auditory 
gyrus  ")  and  in  the  adjacent  posterior  end  of  the  first  temporal 
convolution ;  the  visual  word-centre  (in  individuals  who  have 
learned  to  read)  is  in  the  angular  gyrus.  Either  centre  may 
be  diseased  ;  so  that  we  have  two  varieties  of  sensory  aphasia, 
viz. — auditory  aphasia    and    visual  aphasia.      Then    there    is    in 


108  NERVOUS    DISEASES 

speech  the  motor  element,  consisting  of  the  motor  act  of  expressing 
ourselves  in  words,  either  vocally  or  by  means  of  writing.  The 
memories  of  these  motor  acts  of  vocal  speech  are  usually  sup- 
posed to  be  stored  up  at  the  posterior  end  of  the  inferior  frontal 
(Broca's)  convolution,  and  in  the  adjacent  part  of  the  pre-central 
convolution  and  of  the  insula.  If  this  centre  be  destroyed,  motor 
aphasia  or  aphemia  results,  the  patient  being  unable  to  utter  words 
of  which  his  motor  memories  have  been  destroyed. 

Marie,  however,  has  recorded  cases  of  destruction  of  Broca's 
convolution  without  any  speech  defect,  and  denies  that  it  has  any . 
special  importance  in  the  mechanism  of  speech.  He  considers  that 
cases  of  so-called  motor  aphasia  are  really  examples  of  ordinary 
sensory  aphasia  combined  with  articulative  difficulty  (anarthria  or 
dysarthria)  due  to  a  lesion  of  the  lenticular  nucleus  and  its  surrounding- 
white  matter ;  and  maintains  that  isolated  lesions  of  Broca's  convolu- 
tion are  accidental  and  of  minor  significance. 

Earlier  writers  used  also  to  describe  a  separate  centre  for 
writing  (independent  of  the  vocal  word-centre),  a  lesion  of  which 
would  produce  loss  of  the  faculty  of  writing — -agraphia.  But  no 
case  has  been  verified  pathologically  in  which  a  focal  lesion  has 
produced  pure  agraphia  without  affection  of  vocal  speech,  so  that 
the  writing-centre,  although  it  may  be  represented  diagram- 
matically  in  a  theoretical  scheme  of  cortical  speech-centres,  is 
probably  merely  a  part  of  the  ordinary  psycho-motor  centre  for 
the  upper  extremity. 

Fig.  51  is  a  scheme  of  the  connection  of  the  various  centres 
concerned  in  speech.  Let  us  first  notice  that  the  motor  vocal 
word-centre  is  subservient  to  the  auditory  word-centre,  and  that 
the  writing-centre  is  similarly  subservient  to  the  visual  word- 
centre.  A  child  first  learns  to  speak  by  hearing  spoken  words 
and  then  imitating  them.  Therefore  speech  is  at  first  entirely 
auditory  in  origin.  Later,  in  learning  to  read,  the  meaning  of  each 
word  is  learned  by  associating  the  letters  seen  with  words  heard 
spoken,  so  that  the  auditory  word-centre  acts  as  the  instructor  of 
the  visual  word-centre. 

In  most  people,  during  the  process  of  silent  thought,  words 
are  revived  primarily  in  the  auditory  word-centre,  and  there  is 
usually  a  simultaneous  revival  of  the  same  words  in  the  visual 
word-centre.  But  in  other  people  the  revival  in  the  visual  word- 
centre  comes  to  be  of  greater  importance.  Accordingly  we  may 
classify  people  into  "  auditives  "  and  "  visuals  "  according  to  their 


APHASIA 


109 


mode  of  revival  of  words  in  thought.  Most  of  us  are  "  auditives." 
Simultaneous  revival  of  word-images  in  several  speech-centres 
makes  our  comprehension  of  the  idea  more  perfect.  Thus  a 
difficult  concept  is  better  understood  if  we  read  it  aloud,  because 
this  involves  the  activity  of  the  visual,  auditory  and  vocal 
word-centres. 

Aphasia  commonly  results  from  organic  disease  of  one  or  more 
of  the  cortical  speech-centres,  or  of  the  sub-cortical  fibres  connect- 
ing them.  The  most  frequent  organic  causes  are  embolism,  hsemor- 
rhage,  or  thrombosis,  cerebral  abscesses  and  cerebral  tumours.    The 


FlG.  51. — Diagram  of  Speech-Centres  (after  Bramwell). 

A.  Auditory  word-centre.  V.  Visual  word-centre. 

Sp.  Motor  vocal  word-centre.        W.  Motor  centre  for  writing. 
HV.  Half-vision  centre. 

The  interrupted  lines  indicate  possible  but  less  habitual  routes  for  transmission  of  impulses. 

differential  diagnosis  between  these  various  conditions  depends 
largely  on  the  history ;  embolism  producing  the  symptoms  suddenly, 
haemorrhage  taking  several  minutes,  thrombosis  taking  perhaps 
hours,  abscesses  being  more  gradual  in  onset  and  tumours  still 
more  so.  But  we  also  meet  with  cases  of  temporary  or  functional 
aphasia,  sometimes  from  mere  debility  or  exhaustion,  sometimes 
from  localised  vascular  spasm,  sometimes  following  a  ''  congestive 
attack  "  in  general  paralysis  or  an  epileptic  fit,  or  accompanying 
a  paroxysm  of  migraine,  or  an  attack  of  uraemia. 

In  investigating  a  case  of  aphasia  we  should  first  note  whether 
the  patient  has  other  signs  of  gross  cerebral  lesion,  such  as 
hemianopia,  or  hemiplegia,  and  should  inquire  whether  he  is 
naturally  right-  or  left-handed.     Most  children  are  taught  to  write 


110  NERVOUS    DISEASES 

witli  the  right  hand,  whether  they  are  right-handed  or  not,  and 
therefore  in  determining  this  point  we  inquire  with  which  hand 
a  man  draws  a  cork,  throws  a  stone,  &c.  ;  or  if  a  woman,  with 
which  hand  she  combs  her  hair  or  threads  a  needle ;  or,  in  either 
sex,  which  hand  is  used  in  cutting  bread. 

The  following  series  of  inquiries  (based  on  Beevor's  scheme) 
should  then  be  made.  The  capital  letters  in  parenthesis  indicate 
the  parts  of  the  brain  involved  in  each  case. 

1.  Can  the  patient  spontaneously  utter  intelligible  words  ? 
(Sp.)  Note  the  extent  of  his  vocabulary.  Can  he  pronounce  all 
words  or  only  a  few  ?  Get  the  patient  to  talk  spontaneously,  and 
observe  whether  he  talks  fluently  or  misplaces  words  or  syllables, 
whether  he  talks  in  disjointed  phrases  ("  telegraphic "  type  of 
speech),  or  whether  he  talks  unintelligible  jargon. 

2.  Can  he  understand  words  which  he  hears  ?  (A.)  Ask  him 
to  touch  his  nose,  ear,  eye,  chin,  &c.,  in  turn,  thus  testing  his 
interpretation  of  nouns.  Then  ask  him  to  smile,  whistle,  shut 
his  eyes,  &c.,  thus  testing  his  comprehension  of  verbs.  Some- 
times we  find  that  the  patient  executes  the  first  command  correctly, 
but  continues  to  repeat  the  same  act  in  response  to  different 
commands.  A  patient  can  sometimes  sing  the  words  and  air  of 
a  song,  when  he  is  unabb  to  repeat  the  words  in  a  speaking  voice. 

3.  Can  he  understand  written  questions  or  commands  which 
he  sees  ?  (V.)  Write  down  and  show  him  simple  sentences,  such 
as  "  How  old  are  you  ?  "  "  Put  out  your  tongue."  "  Give  me 
your  left  hand." 

4.  Can  he  write  spontaneously  ?  (W-)  If  his  right  hand  is 
paralysed,  let  him  try  with  the  left.  Observe  whether  he  writes 
intelligibly,  whether  he  misplaces  words  or  syllables,  or  whether  he 
scribbles  meaningless  signs. 

5.  Can  he  copy  from  printed  to  written  letters  ?  (V^W.) 
Print  some  word  such  as  "  Hospital  "  or  "  Monday,"  and  get  him 
to  copy  this. 

6.  Can  he  write  to  dictation  words  which  he  hears  ?    (A^V-^W.) 

7.  Can  he  pick  out  objects  of  which  he  hears  the  name  ? 
(A-*V.)  Place  in  front  of  him  a  heap  of  objects,  such  as  a  key, 
a  shilling,  a  match,  a  pencil,  and  ask  him  to  pick  out  each  in  turn. 

8.  Can  he  repeat  words  heard  ?  (A-*Sp.)  Try  him  first  with 
simple  words  and  phrases  ;  e.g.  "  cat,"  "  dog,"  "  nurse,"  "  good- 
morning,"  &c. 


APHASIA  11] 

9.  Can  he  name  objects  seen,  and  can  he  read  aloud  from  words 
shown  to  him  ?  (V^A-^Sp)  Point  to  different  objects  and  ask 
him  what  they  are. 

10.  Does  he  understand  gestures  and  pantomimic  movements  ? 
Without  speaking  to  him,  get  him  to  imitate  you  when  touching 
the  nose,  spreading  out  the  fingers,  protruding  the  tongue,  &c. 

Auditory  Aphasia,  or  Word-Deafness. — The  patient  in  this 
case  is  not  deaf,  but  simply  word-deaf.  He  hears  ordinary  sounds 
and  noises,  but  spoken  words  are  not  understood ;  they  sound  to 
him  like  an  unknown  tongue.  The  character  of  the  symptoms 
varies  according  as  the  lesion  is  subcortical  or  cortical  in  position, 

(a)  Subcortical,  or  Pure  Auditory  Aphasia.— This  is 
extremely  rare  (Marie,  in  fact,  denies  its  existence).  Here  the 
lesion  simply  blocks  the  way-in  for  spoken  words.  The  patient 
therefore  has  word-deafness — i.e.  he  is  unable  to  understand  what 
is  said  to  him  ;  he  is  also  unable  to  repeat  spoken  words  or  to  write 
from  dictation.  But  the  auditory  word-centre  being  still  intact,  he 
possesses  all  his  memories  of  auditory  speech,  and  therefore 
spontaneous  speech  is  perfect.  Moreover,  the  visual  word-centre 
being  in  normal  working  order,  he  is  still  able  to  read,  and,  as 
a  matter  of  fact,  reading  is  his  only  means  of  receiving  messages 
from  other  people. 

(6)  Cortical  Word-Deafness. — This  is  much  commoner  than 
the  other  variety.  Here  the  lesion  involves  the  cortical  centre  itself, 
and  the  auditory  memories  of  spoken  words  are  obhterated.  And 
therefore,  in  addition  to  the  previous  defects  of  word-deafness  with 
inability  to  repeat  spoken  words  or  to  write  from  dictation,  there 
are  other  symptoms  due  to  the  fact  that  the  motor  speech-centre  is 
no  longer  controlled  by  the  auditory  word-centre.  Internal  speech 
and  thought  are  impaired,  and  so  the  patient  makes  mistakes 
whether  in  speaking  spontaneously  or  in  reading  aloud.  He  also 
makes  mistakes  in  writing,  especially  in  spelling.  He  talks  fluently 
enough,  it  is  true,  but  he  tends  to  mix  up  "his  words  or  syllables, 
and  in  a  severe  case  may  jabber  unintelligible  jargon.  Word- 
deafness  renders  the  patient  unaware  of  his  own  errors.  This,  as 
we  shall  see,  is  in  marked  contrast  with  motor  aphasia,  where  the 
patient  recognises  his  own  mistakes  as  soon  as  he  has  uttered 
them.  If  the  lesion  of  the  auditory  word-centre  be  incomplete, 
the  word-deafness  and  resulting  errors  of  speech  are  also  partial. 


112  NEEVOUS    DISEASES 

These  latter  may,  in  a  slight  case,  be  confined  to  inability  to  name 
objects,  i.e.  nouns,  the  patient  being  still  able  to  express  abstract 
ideas.  Thus  a  partially  word-deaf  patient,  who  is  unable  to  name 
a  knife  shown  him,  may  say,  "  It  is  for  cutting."  Or  again,  partial 
word-deafness  may  produce  simply  confusion  of  words  ;  the  patient 
may  say  one  word  when  he  means  another  (par -aphasia).  It  rarely 
happens  that  word-deafness  remains  permanent  and  complete  ;  the 
auditory  word-centre  in  the  opposite  hemisphere  generally  com- 
pensates, to  some  extent,  as  time  goes  on. 

The  extent  of  mental  disturbance  in  word-deafness  varies  accord- 
ing to  whether  the  patient  be  a  strong  "  auditive  "  or  a  strong 
"visual.  '  In  the  latter  case  the  mental  impairment  is  much  less  than 
in  the  former,  and  the  disturbances  of  motor  speech  are  but  shght. 

The  auditory  and  visual  word-centres  are  fairly  close  together, 
and  more  than  this,  they  are  supplied  by  the  same  branch  of  the 
middle  cerebral  artery  (see  Fig.  32,  p.  50)  ;  so  that  it  is  not  un- 
common for  a  single  arterial  lesion,  e.g.  a  thrombosis,  to  affect  both 
centres  together  and  to  produce  a  combination  of  word-deafness 
and  word-blindness. 

Visual  Aphasia,  or  Word-Blindness  (Alexia). — In  word-blind- 
ness the  patient  can  see,  but  cannot  understand,  printed  or  written 
characters.  They  appear  to  him  hke  strange  hieroglyphics.  He  sees 
the  shape  of  the  letters,  but  they  convey  no  meaning  to  his  mind. 

Here,  as  in  word-deafness,  the  symptoms  vary  in  degree.  The 
patient  may  be  unable  to  recognise  a  single  letter  (letter-blindness), 
or  he  may  be  able  to  spell  out  the  letters  singly  but  unable  to  read 
syllables  or  words.  Often  a  patient  who  is  unable  to  read  any 
other  word,  can  recognise  his  own  name.  Frequently  he  retains 
the  power  of  recognising  numbers  and  of  doing  addition,  sub- 
traction, and  multiplication  sums.  We  have  to  recognise  two 
varieties  of  word-bhndness,  according  as  the  lesion  is  cortical  or 
subcortical  in  position. 

(a)  Subcortical,  or  Pure  Word-Blindness. — Here  the  way- 
in  for  visual  word-impression  is  destroyed,  the  visual  word- 
centre  remaining  intact.  The  patient  cannot  understand  written 
or  printed  words,  nor  can  he  read  aloud,  but  he  still  retains 
the  power  of  writing  spontaneously  and  from  dictation ;  and 
therefore  he  can  express  his  thoughts  perfectly  in  writing,  but 
is  unable  to  read  what  he  has  himself  written.  Inasmuch  as 
a  subcortical  lesion,  in  order  to  produce  word-bhndness,  must  be 


APHASIA 


113 


beneath  the  angular  gyrus  and  in  such  a  position  as  to  cut  off  the 
afferent  visual  impulses  from  both  half-vision  centres  to  the  visual 
word-centre  in  the  angular  gyrus,  it  will  necessarily  imphcate  the 
optic  radiation  to  some  extent.  And  therefore  a  pure  or  subcortical 
word-blindness  is  always  associated  with  (right-sided)  hemianopia 
or,  when  partial,  with  (right-sided)  hemi-achromatopsia  (Fig.  52). 

(6)  Cortical  Word-Blindness. — In  this  variety,  in  addition  to 
the  symptoms  just  described,  there  is  loss  of  the  memories  of  written 
or  printed  words,  and  therefore,  inasmuch  as  the  visual  word-centre, 
which  controls  the  writing-centre,  is  destroyed,  the  patient  has 
agraphia.     He  is  unable  to  write  spontaneously,  to  copy  from  printed 

c.c. 


Fig.  52. — Diagram  representing  a  lesion  (indicated  by  thick  black  line) 
which  produces  pure  word-blindness  (Bastian). 

C.  C.  Posterior  extremity  of  corpus  callosum. 

c.  c.     Commissural  fibres  conuecting  the  two  visual  word-centres. 

b.  b.     Fibres  connecting  each  half-vision  centre  with  the  visual  word-centre  of  the  same  side. 

into  written  characters,  or  to  write  from  dictation.  If  the  lesion 
of  the  visual  word-centre  be  partial  the  alexia  and  agraphia  are 
also  incomplete,  and  mistakes  in  writing  may  amount  simply  to 
the  writing  of  wrong  words,  syllables  or  letters — so-called  "  par- 
agraphia." 

These  points  are  illustrated  by  Bramwell's  well-known  diagram 
(Fig.  51),  in  which  a  lesion  at  the  position  marked  1,  destroying 
fibres  passing  from  one  half-vision  centre  to  the  visual  speech- 
centre,  would  not  produce  word-bhndness.  A  lesion  at  1,  destroy- 
ing fibres  passing  from  both  half -vision  centres  to  the  visual  speech- 
centre,  would  produce  word-blindness  but  not  agraphia,  since  the 
visual  speech- centre  is  unaffected  and  is  able  to  influence  the 
motor  writing-centre.  A  lesion  at  2,  destrojdng  the  visual  speech- 
centre,  would  produce  word-blindness  and  agraphia.  A  lesion  at 
3  would  produce  agraphia  (unless  the  motor  writing-centre  could 

H 


114  NEKVOUS    DISEASES 

be  brought  into  action  in  some  roundabout  way),  but  not  word- 
blindness,  the  visual  speech-centre  being  intact. 

Motor  Aphasia. — In  this  variety  the  patient  has  lost  the 
power  of  expressing  himself  by  spoken  words.  He  can  neither 
speak  spontaneously  nor  can  he  read  aloud.  And  yet  (unless  the 
motor  speech-centres  on  both  sides  of  the  brain  are  destroyed)  he 
is  not  absolutely  dumb.  As  Hughhngs  Jackson  puts  it,  the  patient 
is  speechless,  but  as  a  rule  not  wordless.  He  can  usually  utter 
intelUgently  a  few  words,  such  as  "  yes  "  and  "  no,"  by  means  of 
the  speech-centre  on  the  uninjured  side,  and  in  addition  he  may 
have  other  words  or  phrases,  mostly  interjections,  such  as 
"  oh  my  !  "  "  come  on  !  "  "  damn  !  "  "  by  Jove  !  " — so-called 
"  recurrent  utterances " — ^which  he  utters  automatically  when 
excited,  or  when  making  an  effort  to  speak.  A  patient  who 
has  motor  aphasia,  unlike  a  word-deaf  person,  is  conscious  of  his 
own  errors. 

(a)  Subcortical,  or  Pure  Motor  Aphasia. — Here  the  patient, 
though  intelUgent  and  able  to  understand  spoken  and  written 
language  (by  means  of  his  uninjured  auditory  and  visual  word- 
centres),  cannot  utter  spoken  language,  either  spontaneously  by 
reading  aloud  or  by  repeating  what  he  hears.  This  is  because 
the  way-out  for  spoken  speech  is  blocked.  But  his  mental  speech- 
processes  are  unimpaired,  and  if  the  outgoing  fibres  from  the 
writing  centre  are  unimpaired,  he  is  able  to  express  himself  in 
writing,  as  in  the  biblical  case  of  Zacharias,  the  father  of  John 
the  Baptist  (St.  Luke,  i.  62,  63),  and  in  many  cases  the  patient 
can  indicate  by  signs  how  many  syllables  or  letters  are  in  the 
word  which  he  desires  to  speak  but  cannot  utter.  This  variety  of 
aphasia  sometimes  occurs  in  hysteria.  The  hysterical  aphasic 
cannot  utter  any  sound  whatever,  whether  articulate  or  not. 
Zacharias  was  probably  a  hysterical  aphasic.^ 

(6)  Cortical  Motor  Aphasia. — This  type,  in  which  the  lesion  is 
supposed  to  be  limited  to  the  cortical  motor  speech-centre  in  the 
inferior  frontal  gyrus  and  adjacent  grey  matter  of  the  insula  and 
pre-central  gyrus,  is  less  securely  established  than  the  other  varieties. 
(Marie  denies  its  existence  altogether.)  The  patient  in  this  variety 
has  not  only  all  the  defects  of  a  subcortical  case,  which  we  have 
just  considered,  but,  in  addition,  his  niental  processes  of  internal 

^  "  And  his  mouth  was  opened  immediately,  and  his  tongue  loosed,  and  he 
spake,  and  praised  God." 


APHASIA  115 

thought  are  impaired,  since  the  co-ordination  of  memories  of  words 
spoken  and  written  by  himself  is  impaired.  He  has  therefore 
difficulty  in  understanding  complicated  sentences,  whether  spoken 
or  written.  Together  with  difficulty  in  vocal  speech  there  is  often 
(though  not  always)  associated  a  similar  difficulty  in  writing — 
agraphia — proportional  to  the  defect  of  speech. 

Pure  isolated  agraphia,  without  any  other  symptom,  does  not 
occur,  and  as  we  have  seen,  the  commonest  variety  of  agraphia 
is  that  due  to  cortical  word-blindness.  The  study  of  agraphia  due 
to  sensory  aphasia  is  easier  than  that  associated  with  motor  aphasia, 
because  in  sensory  aphasia  there  is  no  necessary  motor  paralysis 
of  the  right  arm  or  hand,  whereas  sometimes  in  motor  aphasia  the 
patient  has  to  make  his  attempts  at  writing  with  the  left  hand. 

Such  are  the  chief  types  of  aphasia.  Clinically,  however,  it  is 
commoner  to  meet,  not  with  pure  auditory,  visual,  or  motor 
aphasia,  due  to  a  small  focal  lesion,  but  with  combinations  of 
these,  or  with  total  aphasia,  the  result  of  a  larger  destructive 
lesion  implicating  several  or  all  of  the  speech-centres.  Such  severe 
aphasias,  of  course,  produce  a  more  profound  degree  of  mental 
deficiency,  and  inasmuch  as  the  same  artery,  the  middle  cerebral, 
supplies  not  only  the  speech-centres,  but  also  the  other  cortical 
motor  areas  and  the  corpus  striatum  (see  Figs.  32  and  33),  total 
aphasia  is  usually  combined  with  severe  right  hemiplegia. 

Hysterical  aphasia  is  usually  accompanied  by  other  stigmata  of 
hysteria,  and  especially  by  hysterical  hemiplegia.  It  is  paradoxical 
and  polymorphic,  and  usually  differs  from  organic  aphasia  in  some 
curious  fashion,  according  to  the  caprice  of  the  patient.  Thus, 
for  example,  a  patient  with  hysterical  aphasia  may  also  have 
peculiar  tricks  of  intonation  or  of  accent. 

Marie,!  whilst  admitting  tlie  existence  of  visual,  auditory  and  motor 
aphasia  as  clinical  syndromes,  denies  the  existence  of  diagrammatic  visual, 
auditory  and  motor  speech-centres,  and  attributes  all  aphasic  phenomena  to 
intellectual  deficiency  from  disintegration  of  some  part  of  Wernicke's  zone 
(which  consists  of  the  gyri  surrounding  the  extremities  of  the  Sylvian  and 
the  parallel  fissure),  which  zone  he  regards  as  an  intellectual  area.  According 
to  Marie  the  essential  fact  of  aphasia,  of  whatever  variety,  is  insufficient  com- 
prehension of  sj^eech.  He  adduces  evidence  to  show  that  Broca's  convolution 
plays  no  special  part  in  the  function  of  speech  except  in  so  far  as  it  contains 
certain  motor  centres  for  the  face,  tongue  and  larynx.  In  fact  he  discards  a 
s]jecial  vocal-word-centre  just  as  others  discard  a  motor  centre  for  writing. 
The  syndrome  of  motor  aphasia  is  explained  by  him  as  due  to  intellectual 
deficiency  |)Z?is  articulative  anarthria,  this  latter  being  due  to  a  lesion  of  the 

1  Semaine  Medicate,  1906,  Nos.  21,  42,  and  48. 


116  NERVOUS    DISEASES 

lenticular  zone  (comprising  the  lenticular  nucleus  and  its  surrounding  white 
matter).  In  other  words^  he  regards  motor  ajahasia  simply  as  a  sensory- 
aphasia  minus  the  power  of  speech.  The  intellectual  processes  of  speech  in 
right-handed  patients  are  localised  in  the  left  hemisphere,  whereas  anarthria 
may  be  produced  by  a  lesion  of  either  lenticular  zone. 

But  though  seductive  in  their  simplicity,  there  are  certain  obstacles 
to  accepting  Marie's  views  in  their  entirety.  Even  supposing  that  the 
only  real  varieties  of  aphasia  are  sensory,  and  that  some  defect  of  intelli- 
gence is  present  in  every  case,  it  seems  none  the  less  probable  that  visual  and 
auditory  speech-centres  do  exist,  and  that  lesions  of  these  centres,  rather  than 
mere  intellectual  deficiency,  are  the  cause  of  the  well-defined  clinical  types  of 
sensory  aphasia.  As  Dejerine  has  urged,  we  may  have  advanced  dementia 
from  undoubted  cortical  disease,  as  in  general  paralysis,  without  any  aphasia, 
sensory  or  motor.  It  therefore  seems  probable  that  the  diminution  of 
intelligence  which  is  seen  in  aphasic  patients  is  due  to  interference  with 
cortical  sensorial  processes,  producing  disruption  of  the  cerebral  mechanism  of 
sj^eech,  rather  than  that  the  aphasic  phenomena  should  be  regarded  as  secondary 
to  intellectual  defect.  With  regard  to  Marie's  conception  of  motor  aphasia 
as  a  mere  combination  of  intellectual  deficiency  with  anarthria,  it  may  be 
objected  that  this  fails  to  account  for  the  j^resence  of  well-articulated  "  re- 
current utterances"  such  as  are  present  in  most  patients  with  complete  motor 
aphasia.  If  anarthria  alone  were  the  cause  of  the  speech-loss,  it  ought  to 
render  the  articulation  of  all  words  difficult.  Moreover,  the  cortical  vocal- 
word-centre  is  not  limited  to  Broca's  convolution,  but  probably  extends  into 
the  insula  and  to  the  neighbouring  part  of  the  pre-central  gyrus.  So  that 
there  is  no  insuperable  difficulty  in  the  existence  of  a  lesion  limited  to  Broca's 
convolution  unaccompanied  by  aphasia. 

Apraxia  is  the  inability  to  execute  certain  familiar  purposive 
movements  with  the  Kmbs,  when  there  is  neither  motor  paralysis, 
sensory  disturbance,  nor  ataxia  of  the  hmb,  nor  any  intellectual 
impairment.  It  is  tested  by  handing  the  patient  objects — such 
as  scissors,  key,  comb,  drinking-glass,  button-hook,  a  pack  of  cards, 
a  box  of  matches,  &c. — and  observing  whether  he  knows  how  to 
use  them.  Apraxia  of  the  muscles  of  the  limbs  is  analogous  to 
motor  aphasia  of  the  speech  muscles.  Certain  functions,  com- 
parable to  the  functions  of  speech,  have  their  cortical  centres 
situated  in  the  first  and  second  frontal  gyri  of  the  left  hemisphere, 
these  centres  being  connected  with  the  corresponding  centres  in 
the  right  hemisphere  by  means  of  the  anterior  fibres  of  the  corpus 
callosum. 

Apraxia  may  be  either  sensory  or  motor  in  type.  Thus  if  an 
apraxic  patient  be  handed  a  tooth-brush  and  asked  to  use  it,  he 
may  put  it  in  his  mouth  and  try  to  smoke  it  like  a  cigar.  Such 
apraxia  is  sensory  in  origin,  due  to  failure  of  recognition  (agnosia). 
On  the  other  hand,  suppose  he  recognises  it  as  a  tooth-brush 
and  that  he  may  even  name  it  and  tell  what  it  is  for,  but  when 
asked  to  use  it  he  fumbles  aimlessly  with  it,  his  apraxia  is  motor 


APHASIA 


117 


in  type.  To  take  another  example,  motor  apraxia  of  the  tongue 
is  often  seen  in  a  hemiplegia  patient  who  fails  to  protrude  his 
tongue  when  told  to  do  so,  but  can  still  lick  his  Ups  unconsciously. 
Sometimes  the  apraxic  patient  cannot  perform  a  given  series  of 
purposive  movements  unless  he  has  the  sensory  stimulus  of  the 
object  in  his  hand,  with  which  the  movements  are  associated. 
For  example,  an  apraxic  cornet-player  could  not  purse  up  his 
lips    to    blow    the    instrument 


ictual 


Right 


Left  Hand_ 


Right  Hand 


J^' 


unless     he      had     the 
mouthpiece   at  his  Ups. 

Over  95  per  cent,  of 
people  are  right-handed.  In 
them  the  left  cerebral  hemi- 
sphere is  the  dominant  one 
and,  besides  controlling  the 
limbs  of  the  right  side  of  the 
body,  it  exercises  a  potent 
influence  upon  the  right  cere- 
bral hemisphere  by  means  of 
the  commissural  fibres  of  the 
corpus  callosum.  Thus  many 
movements  of  the  left  hmbs 
are  initiated  by  the  left  hemi- 
sphere, so  that  a  left-sided 
cortical  or  subcortical  lesion, 
if  implicating  the  corpus  cal- 
losum, may  produce  not  only  right-sided  hemiplegia  or  mono- 
plegia, but  also  apraxia  of  the  non-paralysed  left  hand.  Such 
apraxia  of  the  ipso-lateral  hand  is  evidence  of  a  lesion  of 
the  fibres  of  the  corpus  callosum.  Apraxia  is  associated  with 
lesions  of  the  left  hemisphere  much  oftener  than  with  right- 
sided  lesions. 

Fig.  53  is  a  diagrammatic  representation  of  the  above-mentioned 
points,  which  shows  that : — 

1.  A  left-sided  cerebral  lesion  at  or  close  beneath  the  arm- 

centre  produces  right  monoplegia  or  hemiplegia,  whilst  the 
left  arm  becomes  apraxic. 

2.  A  lesion  of  the  left  internal  capsule,  where  the  commissural 

fibres  are  uninjured,  causes  right-sided  hemiplegia,  without 
apraxia. 


Fig.  53. — Diagram  illustrating    relation 
of  corpus  callosum  to  apraxia. 


118  NERVOUS    DISEASES 

3.  A  lesion  of  the  corpus  caUosum  (or  of  the  left  centrum  ovale 

implicating  callosal  fibres)  will  cause  left-sided  apraxia 
(from  loss  of  the  guidance  of  the  left  arm-centre  over  the 
right),  without  hemiplegia  on  either  side. 

4.  A  lesion  of  the  right  frontal  lobe  may  interrupt  the  callosal 

fibres  passing  from  the  left  to  the  right  arm-centre  without 
injuring  the  pyramidal  fibres  from  the  right  centre 
to  the  left  hand.  In  such  a  case  we  have  a  left-sided 
apraxia  from  a  right-sided  lesion. 


CHAPTER   VIII 

DISORDERS   OF  ARTICULATION 

It  is  necessary  to  distinguish  clearly  between  speech  and  articula- 
tion.    Speech  is  a  cortical  function,  articulation  is  mainly  bulbar. 

Disordered  articulation,  or  dysarthria,  signifies  difficulty  in  per- 
forming the  co-ordinated  muscular  movements  necessary  for  the 
production  of  the  consonants  and  vowels  which  go  to  form  syllables 
and  words. 

In  simple  dysarthria  there  is  no  afiection  of  the  cortical 
centres  or  paths  which  are  concerned  in  the  processes  of  speech 
proper.  A  patient,  for  example,  who  has  advanced  bulbar  palsy, 
even  when  he  is  unable  to  articulate  a  single  word,  is  not,  strictly 
speaking,  speechless.  He  is  inarticulate,  which  is  quite  a  different 
thing.  His  mental  speech-processes  remain  normal,  he  can  still 
express  himself  fluently  in  written  speech,  and  he  is  able  to  under- 
stand everything  he  hears  or  sees. 

The  peripheral  mechanism  of  vocal  speech  is  partly  musical 
(or  voiced),  consisting  in  vibration  of  the  approximated  vocal 
cords.  It  is  also  partly  consonantal  (or  voiceless),  consisting  in 
the  co-ordinated  action  of  numerous  muscles  of  the  Ups,  tongue, 
palate,  and  pharynx.  The  term  "  articulation  "  is  specially  applied 
to  the  mechanism  of  consonantal  pronunciation. 

To  test  a  patient's  power  of  articulation,  we  listen  to  his 
ordinary  conversation,  or  we  ask  him  to  read  aloud  a  passage 
from  a  book  or  newspaper,  and  notice  how  he  pronounces  his 
words.  Then,  if  he  shows  any  abnormality  in  connection  with 
particular  consonants,  we  ask  him  to  repeat  "  catch "  words, 
chosen  so  as  to  present  special  difficulties,  e.g.  "  British  consti- 
tution," "  biblical  criticism,"  "  West  Register  Street,"  "  hippo- 
potamus," "  Burgess's  fish-sauce  shop,"  "  steel  ratchet  screw- 
driver," &c. 

Difficulties  of  articulation  are  the  result  of  defects,  consisting 
either  in  paralysis  or  inco-ordination,  of  certain  groups  of  muscles 
in  the  lips,  tongue,  palate,  pharynx,  or  larynx.      The  underlying 

119 


120  NERVOUS   DISEASES 

defect  may  either  be  in  the  bulbo-muscular  neurones  (comprising 
the  pontine  and  medullary  nuclei,  the  peripheral  motor  nerves  and 
the  muscles),  or  it  may  be  due  to  supra-nuclear  affections  in  the 
cortico-bulbar  neurones,  at  some  point  between  the  higher  speech- 
centres  and  the  bulbar  nuclei.  Or  it  may  be  due  to  ataxia  of  the 
organs  of  speech. 

Infra-nuclear  and  Nuclear  Affections  of  Articulation. — 
Articulation  may  be  impaired  as  a  result  of  paralysis  of  any  of  the 
motor  nerves  or  nuclei  supplying  the  articulative  muscles. 

Unilateral  hypoglossal  paralysis  (as  in  the  case  of  a  business  man 
shown  in  Fig.  84,  in  whom  this  nerve  was  divided  by  a  stab  in  the 
neck  dealt  by  a  discharged  employe)  produces  motor  paralysis 
followed  by  atrophy  of  the  corresponding  half  of  the  tongue.  The 
paralysed  half-tongue  feels  to  the  patient  as  if  he  had  a  foreign 
body  in  his  mouth.  This  makes  his  articulation  clumsy,  hsping  and 
indistinct,  especially  in  the  case  of  hnguo-dental  (S,  Z,  Th)  and  of 
anterior  hnguo-palatal  consonants  (T,  D,  L,  R).  But  after  a  few  days 
the  patient  becomes  accustomed  to  the  feeling  of  his  palsied  half- 
tongue,  and  his  articulative  difficulty  to  a  large  extent  disappears. 

Facial  palsy,  from  its  affection  of  the  lips,  renders  labials  (P,  B) 
and  labio-dentals  (F,  V)  indistinct,  especially  so  when  the  palsy 
is  bilateral. 

Bilateral  paralysis  of  the  palate,  e.g.  post-diphtheritic  paralysis, 
congenital  cleft  palate,  and  syphiUtic  perforation  of  the  palate, 
all  produce  the  same  articulative  difficulty,  inasmuch  as  the  nasal 
cavity  cannot  be  shut  off  from  the  mouth.  As  a  result  the  voice 
is  nasal,  and  certain  consonants  are  altered  (B  becomes  M,  D  be- 
comes N,  K  becomes  Ng,  and  so  on),  so  that  articulation  as  a 
whole  is  indistinct.  This  indistinctness  of  articulation  is  increased 
when  the  patient  stoops  forwards  :  it  diminishes  or  even  disappears 
on  lying  with  the  head  thrown  backwards,  since  in  the  latter 
position  the  paralysed  soft  palate  tends  to  fall  back  by  its  own 
weight  and  shuts  off  the  naso-pharynx.^ 

Total  paralysis  of  the  palate  is  also  associated  with  difficulty 
in  deglutition,  especially  with  liquids,  which  during  the  act  of 
swallowing  regurgitate  into  the  naso-pharynx  and  escape  through 
the  anterior  nares. 

Unilateral  paralysis  of  the  recurrent  laryngeal  nerve,  if  com- 
plete, renders  the  voice  hoarse,  by  paralysing  one  vocal  cord,  and 

1  Schlesinger,  Neurologisches  Gentralhlatt,  1906,  p.  50. 


DISORDERS    OF    ARTICULATION  121 

so  interfering  with  the  phonation  of  vowels,  but  not  with  the  articu- 
lation of  consonants.  If  the  vagus  root  be  affected  at  its  point  of 
exit  from  the  medulla,  the  soft  palate  is.  often  paralysed  on  the 
same  side  (see  later,  Cranial  Nerves).  But  unilateral  palatal 
palsy,  unlike  bilateral,  does  not  affect  the  articulation  of  con- 
sonants. 

Articulation  may  also  become  indistinct  from  disease  of  the 
bulbar  nuclei — so-called  glosso-labio -laryngeal  paralysis,  or  bulbar 
palsy.  In  this  disease  there  is  a  diffuse,  progressive  weakness  of 
the  muscles  of  articulation,  with  atrophy  and  fibrillary  tremors  of 
the  muscle-fibres,  especially  those  of  the  tongue  and  lips.  Articula- 
tion becomes  more  and  more  indistinct,  saUva  dribbles  from  the 
patient's  trembUng  hps,  and  in  advanced  cases  there  is  interfer- 
ence with  swallowing  and  coughing.  If,  as  is  often  the  case, 
bulbar  palsy  is  an  upward  extension  of  an  amyotrophic  lateral 
sclerosis,  there  may  be  a  concomitant  muscular  atrophy  and 
fibrillary  tremor  in  the  muscles  of  the  upper  Hmbs,  especially 
in  the  intrinsic  hand  muscles.  Owing  to  affection  of  the  pyra- 
midal tracts,  there  is  also  exaggeration  of  the  deep  reflexes  and 
general  spasticity,  especially  of  the  lower  hmbs. 

There  is  a  form  of  myopathy — the  facio-scapulo-humeral  type 
of  Landouzy  and  Dejerine,  in  which  the  facial  muscles  are 
atrophied.  This  affection  is  a  bilateral  one  and  the  patient's 
lower  lip  protrudes  in  a  characteristic  fashion  which  has  been 
termed  the  "  tapir  "  type  of  Up.  He  has  also  a  pecuhar  "  trans- 
verse "  smile.  In  severe  cases  of  this  disease  the  articulation  of 
labial  consonants  becomes  impaired  just  as  it  does  in  double 
facial  palsy. 

Myasthenia  gravis,  when  it  affects  the  bulbar  muscles,  repro- 
duces all  the  features  of  bulbar  palsy,  with  this  difference,  that 
the  paralysis  varies  in  its  degree  from  time  to  time,  becoming 
accentuated  by  fatigue.  After  a  period  of  rest  a  patient  so 
affected  may  resume  with  normal  articulation,  but,  if  he  continues 
to  speak,  his  muscles  gradually  become  exhausted,  and  his  articula- 
tion becomes  more  and  more  indistinct.  Not  only  the  lips  and 
tongue,  but  the  ocular  muscles,  the  muscles  of  mastication  and 
various  muscles  of  the  trunk  and  Hmbs,  show  evidence  of  temporary 
paralysis  or  fatigue,  and  ultimately  the  patient  succumbs  to  fatigue 
of  his  respiratory  muscles. 

Articulative  Ataxia. — There  are  some  diseases  in  which  articu- 


122  NERVOUS   DISEASES 

lation  becomes  indistinct,  not  from  paralysis  of  the  muscles  but 
from  ataxia. 

In  Friedreich'' s  ataxia,  for  example,  the  articulation  becomes 
slow,  thick,  and  clumsy,  and  the  patient  talks  as  if  he  had  a 
foreign  body  in  his  mouth,  so  that  his  speech  has  been  aptly 
termed  the  "  hot-potato  "  speech.  The  pitch  of  the  voice  in  this 
disease  may  vary  from  word  to  word,  and  in  advanced  cases  a 
certain  degree  of  mental  feebleness  is  often  superadded. 

In  laryngeal  tahes  in  which  the  larynx  is  affected  by  ataxy  the 
voice  is  tremulous,  and  when  a  tabetic  patient  has  ataxia  of 
the  tongue  his  articulation  becomes  laboured.  This  lingual  trouble 
in  tabes  is  often  associated  with  a  peculiar  constant  rolling  move- 
ment of  the  tongue  on  the  floor  of  the  mouth,  even  when  the 
patient  is  not  speaking.  The  patient  often  has  an  annoying 
subjective  sensation  in  his  tongue,  as  if  it  were  covered  with 
blotting-paper,  which  he  tries  to  get  rid  of  by  the  restless  rolling 
of  his  tongue. 

Supra-nuclear,  or  Cortico-bulbar  Affections  of  Articulation. 
— Articulation  may  be  afiected  where  the  upper  or  cortico -nuclear 
neurones  are  involved.  The  slurring  articulation  of  many  cases  of 
acute  alcoholic  intoxication  is  familiar  to  lay  observers,  being  especi- 
ally marked  in  the  pronunciation  of  labial  and  of  anterior  linguo- 
dental  consonants.  In  rare  instances  alcoholic  dysarthria  persists 
for  days  after  the  alcoholic  celebration.  ToUmer  and  other  French 
authorities  ascribe  this  circumstance  to  cerebellar  intoxication. 
Many  alcoholic  patients  realise  their  own  articulative  difficulty, 
and  in  endeavouring  to  compensate  for  it,  they  utter  certain 
words  with  a  deliberation  and  undue  emphasis  that  betrays  them. 

Very  similar  to  the  alcohohc  articulation  is  that  of  general 
paralysis  of  the  insane.  But  the  typical  general  paralytic  shows 
also  a  characteristic  fibrillary  tremor  of  all  the  muscles  around 
the  lips  and  nose. 

Both  in  acute  alcoholism  and  in  general  paralysis  there  is 
often  a  tendency  to  choose  an  occasional  wrong  word,  or  to  mis- 
place syllables.  Such  defects  are  not  bulbar  but  cortical  in  origin. 
In  the  later  stages  of  general  paralysis,  articulation  may  be  totally 
unintelhgible,  reduced  to  a  mere  mumble. 

After  an  attack  of  right-sided  hemiplegia,  the  patient  is  often 
aphasic.  But  even  in  a  left-sided  hemiplegia  where  no  true 
aphasia  exists,  it  is  not  uncommon  to  find  a  temporary  change  in 


DISORDERS    OF    ARTICULATION  123 

the  articulation,  which  loses  its  crispness,  and  becomes  somewhat 
laboured  and  indistinct.  This  dysarthria  usually  passes  off  after 
a  few  days,  but  sometimes  persists  permanently,  in  varying  degree, 
especially  if  the  lesion  involves  the  lenticular  nucleus.  A  lesion  of 
the  left  lenticular  produces  greater  dysarthria  than  one  of  the  right 
nucleus.^  The  dysarthria  of  lenticular  disease  is  due  mainly  to 
spasticity.^ 

In  cases  in  which  a  patient  has  a  bilateral  hemiplegia  we  often 
meet  with  "  pseudo-bulbar  "  paralysis.  The  most  common  history 
is  that  there  have  been  one  or  more  hemiplegic  attacks,  all  confined 
to  the  same  side,  but  at  last  the  patient  has  an  attack  on  the 
opposite  side.  This  now  produces,  in  addition  to  the  classic  signs 
of  a  double  hemiplegia,  pseudo-bulbar  paralysis,  with  thick,  in- 
distinct articulation,  closely  resembhng  that  of  true  bulbar  palsy 
and  with  the  same  dribbling  of  saliva,  difficulty  in  swallowing, 
coughing,  &c.,  but  without  atrophy  or  fibrillary  tremors  of  the 
affected  muscles.  The  pseudo-bulbar  patient  is  emotionally 
irritable  ;  he  laughs,  or  more  often  cries,  on  sHght  provocation, 
and,  unhke  the  subject  of  true  bulbar  paralysis,  he  is  generally 
somewhat  deficient  mentally.  There  is  usually  a  history  of 
successive  (more  rarely  of  simultaneous)  attacks  of  hemiplegia 
on  opposite  sides  of  the  body. 

Bilateral  athetosis  is  a  disease  which  is  usually  congenital,  although 
the  symptoms  do  not  necessarily  appear  at  birth,  but  may  begin 
in  childhood  or  even  in  adolescent  life.  The  disease  gradually 
increases  in  severity.  It  is  characterised  by  wild  wriggHng  and 
twisting  movements  of  all  the  limbs,  chiefly  on  attempted  voluntary 
movements  (but  sometimes  spontaneously,  when  no  effort  is  being 
made),  and  by  grimacing  of  the  face,  together  with  spastic  rigidity 
of  the  affected  muscles  (see  Figs.  54  and  55).  There  is  generally 
a  certain  degree  of  mental  deficiency.  The  pyramidal  tracts  are 
not  necessarily  affected,  and  the  plantar  reflexes  are  usually  of  the 
normal  flexor  type.  In  this  disease  articulation  is  often  affected. 
The  grimaces  of  the  face  and  of  the  tongue  muscles  interfere  con- 
siderably with  articulation.  Moreover,  irregular  spasmodic  con- 
tractions of  the  diaphragm  and  other  respiratory  muscles  give 
the  voice  a  curiously  jerky  or  groaning  character,  due  to  sudden 
interruptions  of  breathing. 

^  Mingazzini,  Sulla  sintomatologia  delle  lesione  del  nucleo  lenticolare,  1902. 
2  Wilson,  "  Progressive  Lenticular  Degeneration,"  Brain,  1912. 


124 


NERVOUS   DISEASES 


Patients  suffering  from  disseminated  sclerosis  frequently  liave 
a  peculiar  so-called  "  staccato  "  speech,  in  which,  the  words  are 
enunciated  in  a  jerky  mincing  fashion,  very  difl6.cult  to  describe, 
but  easy  to  recognise  once  it  has  been  heard.  This  is  sometimes 
called  the  "  scanning "  speech,  from  its  fancied  resemblance  to 
the  scansion  of  Latin  or  Greek  verse. 

In  paralysis  agitans,  as  the  disease  advances,  the  patient's 
voice  becomes  thin,  feeble  and   reduced  almost   to  a  monotone, 


Fig.  54. 


Fia.  55. 


Figs.  54  and  55. 
months'  child. 


—Double  athetosis  in  a  girl  of  17.       The  patient  was  a  7^ 
She  had  also  signs  of  stenosis  of  the  pulmonary  artery. 


whilst  his  articulation,  hke  his  gait,  acquires  a  "  festinant "  char- 
acter. When  speaking,  he  begins  slowly,  but  towards  the  ends 
of  sentences  or  long  words  he  tends  to  hurry,  so  that  the  final 
syllables  are  pronounced  hastily.  Together  with  this  we  have  the 
characteristic  "  starched,"  expressionless  face,  the  Parkinsonian 
mask,  commencing  unilaterally  and  ultimately  becoming  bilateral. 

In  severe  cases  of  chorea  the  articulation  may  be  interfered 
with,  owing  to  sudden  violent  movements  of  the  face,  tongue,  and 
respiratory  muscles.  Speech  becomes  hesitating  and  jerky,  and 
in  very  bad  cases  the  voice  may  be  reduced  to  a  whisper. 

There  are  also  affections  of  articulation  due  to  functional 
cortical  disturbances.     Of  these  the  most  familiar  is  stammering, 


DISORDERS    OF    ARTICULATION  125 

commonest  in  individuals  who,  whilst  usually  above  the  average 
intelligence,  have  a  congenital  psychasthenic  tendency.  Stanmaer- 
ing  consists  in  a  want  of  co-ordination  between  the  vocal 
(laryngeal)  and  consonantal  (oral)  mechanisms  of  speech,  so  that, 
in  the  common  type,  the  patient  sticks  at  a  consonant,  which  he 
often  continues  to  repeat,  over  and  over  again,  before  he  finally 
succeeds  in.  enunciating  the  rest  of  the  word.  He  misdirects 
his  energy  on  the  consonants,  instead  of  touching  them  hghtly 
and  passing  on  to  the  vowel  sounds.  Most  stammerers  lose  their 
stammer  when  they  sing,  their  attention  being  then  directed  to 
the  vocal  part  of  speech.  The  vast  majority  of  stammerers  are 
males. 

A  rarer  variety  of  stammering  is  that  in  which  the  patient  sticks 
at  initial  vowels.  This  is  due  to  temporary  spasm  of  the  false 
vocal  cords,  and  the  patient  remains  with  his  mouth  wide  open 
until  the  spasm  relaxes,  when  his  words  suddenly  rush  forth  in  a 
hurried  stream  until  he  has  no  breath  left.  He  then  takes  another 
breath  and  the  precipitate  rush  again  occurs.^ 

Many  stammerers  acquire  various  tricks,  chiefly  through  their 
efforts  to  overcome  the  stammer.  Thus  extra  noises  may  be  thrown 
in,  e.g.  sudden  inspiratory  grunting  or  whooping  noises,  or  the 
patient  may  make  grimaces  or  curious  contortions  of  the  limbs. 

This  leads  us  to  recall  the  various  articulation  tics  or  habit-spasms 
which  are  met  with  in  psychasthenic  patients,  either  in  conjunction 
with  stammering  or  independently  of  it,  and  these  may  be  of  the 
most  varied  character.  The  patient's  speech  may  be  interrupted 
by  weird  pharyngeal  barking  or  grunting  noises.  Or  the  articulation 
may  be  monosyllabic,  a  whole  breath  being  taken  for  each  syllable. 
Or,  again,  it  may  be  jumbled  up  in  the  most  extraordinary  ways, 
though  the  "  tiqueur "  usually  interpolates,  now  and  then,  a 
clearly  articulated  sentence  or  phrase  amongst  other  uninteUigible 
ones.  Hysterical  aphonia  is  fairly  common,  and  can  usually  be 
recognised  by  the  history,  together  with  the  characteristic  laryngeal 
appearances.  We  also  meet  with  cases  of  hysterical  mutism,  in 
which  the  patient  does  not  utter  even  a  whispered  word. 

^  Cathcart  has  pointed  out  that  this  variety  of  stammering  is  described 
in  Shakespeare's  As  You  Like  It  (Act  iii.  Scene  2)  as  follows: — 

"  I  would  thou  couldst  stammer,  that  thou  mightst  pour  out  this  con- 
cealed man  out  of  thy  mouth,  as  wine  comes  out  of  a  narrow-necked  bottle, 
either  too  much  at  once,  or  none  at  all.  I  prithee,  take  the  cork  out  of  thy 
mouth  that  I  may  drink  thy  tidings." 


126  NERVOUS   DISEASES 

Deaf-mutes  are  the  patients  wlio  are  popularly  known  as 
"  deaf  and  dumb."  A  normal  child  learns  to  speak  by  imitating 
words  which  he  hears,  but  if  a  child  be  congenitally  deaf,  he 
does  not  learn  to  speak,  but  remains  deaf  and  dumb.  Moreover, 
if  he  is  born  with  normal  hearing,  but  subsequently  becomes 
deaf,  e.g.  from  middle  ear  disease  or  from  meningitis,  before 
the  age  of  about  six  years,  he  usually  loses  his  power  of  speech. 
Such  deaf-mutes  can  generally  be  taught  to  speak  again  by 
the  oral  or  "  lip-reading  "  method,  where  the  child  imitates  the 
movements  of  his  teacher's  muscles  of  articulation  and  also  learns 
to  phonate,  though  usually  with  a  harsh,  discordant  voice.  But 
even  deaf-mutes  who  have  never  been  taught  to  speak  usually 
make  noises  of  some  sort  or  other,  often  pharyngeal  snorts  and 
grunts,  or  spluttering  labial  noises,  and  less  frequently  laryngeal 
sounds.  They  do  this  especially  when  excited.  This  was  the  case 
with  a  deaf-mute  who  used  to  make  weird  snorting  noises  when 
playing  football.  These  doubtless  helped  to  smite  terror  into  the 
hearts  of  the  opposite  side.  The  congenital  deaf-mute  is  usually 
brighter  and  more  clever  than  the  deaf-mute  whose  deafness  was 
acquired.  Deaf-mutes  generally  have  a  wonderful  command  of 
gestures  and  signs. 

Deaf-mutism  constitutes  a  common  variety  of  war-neurosis 
after  shell-explosions.  The  soldier  is  flung  to  the  ground,  or 
perhaps  even  partially  buried,  by  a  bursting  shell,  and  may  be 
rendered  unconscious,  although  this  latter  is  not  essential.  He 
immediately  finds  himself  mute  or  deaf-mute.  A  considerable 
proportion  of  such  patients  can  be  rapidly  cured  by  suggestion, 
sometimes  aided  by  the  administration  of  a  general  anaesthetic. 

The  dumbness  which  is  present  in  profound  degrees  of  idiocy 
is  not  an  articulative  difficulty,  but  a  true  speech  affection  due 
to  mal-development  of  the  cortical  speech-centres.  An  imbecile 
child  is  speechless  because  he  has  no  ideas  to  express ;  in  this 
respect  he  differs  from  the  deaf-mute,  who  is  often  bright  and 
intelligent. 

Certain  varieties  of  deficient  articulation  are  met  with  in 
children  or  in  adults  who  are  mentally  more  or  less  childish.  The 
condition  known  as  lalling  consists  m  a  want  of  precision  in  the 
pronunciation  of  certain  consonants.  Thus  a  patient  may  substitute 
the  uvular  R  for  the  ordinary  linguo -palatal  R.,  or  he  may  sub- 
stitute V  for  Th  or  W  for  R,  so  that  "  broken  reed  "  becomes 


DISORDERS    OF    ARTICULATION  127 

"  bwoken  weed."  Or,  again,  the  patient  may  substitute  Th  for  S 
and  is  then  said  to  lisp.  These  last  two  varieties  are  sometimes 
voluntarily  assumed,  as  a  fashionable  affectation,  by  young  men 
not  overburdened  with  brain  power.  More  serious  varieties  of  lalling 
are  where  the  letter  L  is  replaced  by  some  other  consonant,  so 
that  "  elephant  "  may  be  pronounced  as  "  edephant,"  "  esephant," 
"  enephant,"  "  erephant,"  &c.  Still  worse  is  it  when  the  patient 
has  difficulty  with  K  or  G,  their  places  being  taken  by  T  and  D 
respectively. 

As  a  general  rule,  it  may  be  stated  that  lalhng  on  a  single 
consonant  does  not  necessarily  indicate  defective  intellect,  whereas 
lalling  on  many  consonants,  if  the  patient  has  passed  the  age 
of  childhood,  should  arouse  the  suspicion  of  mental  deficiency, 
although  lalHng  is  a  normal  stage  in  the  process  of  learning  to 
speak. 

Finally,  there  is  the  condition  known  as  idioglossia,  in  which 
from  difficulty  in  pronouncing  his  consonants  a  child  retains  the 
correct  vowels,  but  substitutes  other  consonants  and  seems  to 
speak  a  new  language  of  his  own.  The  child  is  usually  mentally 
bright  and  understands  all  that  is  said  to  him.  He  talks  volubly 
but  unintelhgibly.  As  a  rule  he  completely  outgrows  the  weak- 
ness in  course  of  time. 


CHAPTER   IX 

CRANIAL    NERVES 

I'he  recognition  of  cranial  nerve  palsies  is,  diagnostically,  of  the 
utmost  importance,  nor  is  it  a  matter  of  such,  difficulty  as  is 
commonly  imagined. 

First,  or  Olfactory  Nerves. — 

From  the  under-surface  of  the  olfactory  bulb  on  each  side  there 
arise  some  twenty  minute  nerves  which  perforate  the  cribriform 
plate  of  the  ethmoid  to  be  distributed  to  the  upper  part  of  the 
nose. 

To  test  the  sense  of  smell,  we  direct  the  patient  to  close  his 
eyes.  We  then  hold  aromatic  substances,  such  as  oil  of  cloves, 
peppermint,  turpentine,  or  asafoetida,  in  front  of  each  nostril  in 
turn,  closing  the  other  nostril  with  the  finger.  Ammonia  or 
acetic  acid  must  not  be  used  to  test  the  sense  of  smell,  since 
these  stimulate  the  fifth  nerve  (common  sensation),  and  may 
produce  a  pungent  sensation  in  the  nose,  even  when  the  sense 
of  smell  is  lost. 

Anosmia,  or  loss  of  the  sense  of  smell,  is  sometimes  of 
diagnostic  value.  It  may  occur,  for  example,  in  congenital  absence 
of  the  olfactory  nerves,  in  lesions  of  the  olfactory  bulb  or  olfactory 
tract,  in  some  frontal  tumours,  in  injuries  of  the  anterior  fossa 
of  the  skull,  and  in  tabetic  atrophy  of  the  olfactory  nerves. 
It  also  very  often  occurs  unilaterally  in  hysterical  hemiplegia  and 
is  then  associated  with  diminution  of  the  other  special  senses  on 
the  hemiplegic  side.  But  the  value  of  anosmia  as  a  symptom  is 
lessened  by  the  fact  that  numerous  local  obstructive  conditions 
in  the  nose  also  produce  loss  of  smell,  e.g.  nasal  polypi  or  even  a 
simple  cold  in  the  head. 

Paros7nia,  or  perverted  sense  of  smell,  is  always  cortical  in 
origin.  Various  subjective  hallucinations  of  smell  occur  not  only 
in  mental  disease  but  also  in  gross  lesions  of  the  uncinate  gyrus, 
which  is  the  cortical  olfactory  centre.  But  here  again  local  nasal 
conditions  may  also  cause  olfactory  sensations,  e.g.  the  unpleasant 

128 


CRANIAL    NERVES 


129 


odour  perceived  by  a  patient  suffering  from  empyema  of  the 
antrum  of  Highmore,  from  which  horribly  offensive  pus  is  escaping 
into  the  nose.  On  the  other  hand,  in  ozsena  from  chronic  atrophic 
rhinitis  the  offensive  smell  Ls  not  perceived  by  the  patient,  although 
painfully  evident  to  his  neighbours. 

Paroxysmal  parosmia,  preceded  by  a  disagreeable  sensation  of 
irritation  at  the  root  of  the  nose,  and  sometimes  followed  by 
violent  sneezing  and  sudden  secretion  of  nasal  mucus,  may  occur 
as  a  nasal  crisis  in  tabes/ 

Second,  or  Optic  Nerve. — This  contains  not  only  visual  fibres, 
but  also  the  afferent  fibres  for  the  pupillary  reflex. 


Fig.  56. — Diagram  of  pons  and  medulla,  showing  cranial  nerves. 

We  have  already  referred  to  the  course  of  the  visual  path  from 
retina  to  cortex  (Fig.  29,  p.  46),  In  testing  vision  we  should 
determine  visual  acuity  by  means  of  test  types  at  a  fixed  distance, 
such  as  six  metres.  Using  Snellen's  types,  of  which  the  largest 
should  be  readable  at  sixty  metres,  and  the  smallest  at  six  metres, 
we  direct  the  patient  to  read  the  letters  from  above  downwards. 
If  his  vision  is  normal  he  will  be  able  to  read  the  smallest  type  at 
six  metres.  His  visual  acuity  is  then  represented  as  V  =  f .  But  if 
he  can  only  read  down  as  far  as  the  type  which  ought  to  be  visible  at 
thirty  metres,  then  V  =  y*^.  Each  eye  should  be  tested  separately, 
the  test  types  being  well  illuminated  and  the  patient  standing 
with  his  back  to  the  light.  When  the  visual  acuity  is  much  im- 
paired, the  patient  may  not  see  even  the  largest  type,  but  can  only 

'  Klippel  and  Lhermitte,  Semaine  Medicah,  Feb.  17,  1909. 


130 


NERVOUS    DISEASES 


count  fingers  at  a  short  distance,  or  perhaps  can  only  tell  Hght 
from  darkness.  Temporary  diminution  of  visual  acuity  may 
occur  in  myasthenia  gravis.-^ 

Hemeralopia,  or  day-blindness,  is  a  condition  in  which  the 
power  of  vision  is  bad  during  the  day  or  in  a  bright  light,  whilst 
the  patient  sees  better  in  a  dim  light.  The  phenomenon  is  not 
uncommon  in  tobacco  amblyopia,  where  there  is  usually  present 
a  central  scotoma  for  green  and  red.  The  hemeralopia  is  pro- 
bably due  to  the  fact  that  a  bright  light  rapidly  fatigues  the 
retina  and  also,  by  producing  pupillary 
contraction,  causes  the  peripheral  part  of 
the  retina  to  be  less  in  use  than  the 
central,  whereas  in  a  dim  light  the  pupil 
dilates  and  the  unaffected  peripheral  por- 
tion of  the  retina  comes  into  play. 

A  patient  with  nyctalopia,  or  night- 
blindness,  becomes  almost  blind  at  dusk  or 
in  a  dim  light.  This  occurs  in  association 
with  various  conditions,  of  which  the  most 
interesting  is  congenital  retinitis  figmentosa, 
a  disease  easily  recognised  on  ophthalmo- 
scopic examination.  It  also  occurs  to  a 
lesser  degree  in  certain  cases  of  "  cortical  " 
cataract,  when  the  lenticular  opacity  acts 
as  a  permanent  diaphragm. 

Colour  vision  is  most  conveniently  tested 
by  means  of  Holmgren's  wools.  These  are 
thrown  on  a  table  weU  lit  by  daylight,  and 
the  patient  is  given  one  particular  test-skein  of  wool  which  is  kept 
separate  from  the  heap,  and  told,  not  to  name  the  colour,  but  to 
match  it,  selecting  from  the  heap  of  coloured  skeins  all  those  which 
are  like  the  test-skein,  whether  lighter  or  darker  in  shade.  The 
patient  is  given  a  pale  green  test-skein.  If  his  colour  vision  is 
normal,  he  will  pick  out  all  the  pale  greens  correctly,  but  if  he  is 
red-green  colour-blind  he  will  select  a  grey  or  straw-coloured  skein. 
Congenital  red-green  colour-blindness  is  the  commonest  variety. 
Yellow-blue  colour-blindness  is  less  common.  If  a  patient  be 
totally  colour-blind  he  will  confuse  with  the  test-skein  all  those 
of  similar  brightness,  no  matter  what  their  colour  may  be. 
^  Tilney  and  Mitchell  Smith,  Neurographs,  1911,  vol.  i.  p.  178. 


Fig.  57. — Lateral  view  of 
brain-stem  with  cra- 
nial nerves. 


CRANIAL    NERVES  131 

The  size  of  the  field  of  vision  in  each  eye  is  of  great  importance, 
and  for  its  accurate  measurement  a  perimeter  is  required.  This, 
however,  is  a  large  and  expensive  piece  of  apparatus.  For  clinical 
purposes  the  following  method  is  sufficient,  presuming  that  the 
physician's  own  visual  fields  are  normal.  The  physician  sits  exactly 
opposite  the  patient,  about  a  yard  away  from  him,  and  tests  each 
eye  separately.  To  test  the  patient's  right  eye  direct  him  to  cover  up 
his  left  and  to  gaze  steadily  at  the  physician's  left  eye.  Meanwhile 
the  physician  closes  his  own  right  eye  and  looks  steadily  at  the 
patient's  pupil,  watching  that  the  patient's  eye  does  not  wander 
from  the  fixation  point.  Then,  holding  his  own  left  hand  in 
a  plane  midway  between  himself  and  the  patient,  and  beginning 
almost  at  arm's-length,  he  brings  his  hand  inwards  from  the 
patient's  ear  towards  the  middle  Hne,  meanwhile  moving 
his  own  fingers.  If  the  patient's  visual  field  is  normal,  he 
will  catch  sight  of  the  moving  fingers  at  the  same  time  that 
the  physician  does  so.  If  he  does  not,  that  visual  field  is 
contracted  and  the  physician  then  brings  his  moving  fingers 
inwards  until  the  patient  does  catch  sight  of  them.  In  this 
way  we  test  both  the  upper  and  lower  quadrants  of  the 
field  on  the  temporal  and  nasal  sides,  in  turn.  If  we  find 
the  visual  field  diminished  in  one  or  other  eye,  it  is  well  to 
take  a  careful  perimetric  chart. 

We  may  find  a  central  scotoma  or  blind  patch  in  one  or  both 
visual  fields.  This  is  detected  by  attaching  a  small  white  object 
to  the  end  of  a  thin  rod  and  holding  it  in  the  centre  of  the  visual 
field,  midway  between  one's  own  and  the  patient's  eye.  In  this 
situation  it  is  not  seen  by  the  patient.  We  gradually  move  the 
white  object  radially  outwards  in  various  directions  until  the 
patient  catches  sight  of  it.  Central  scotoma  may  occur  in  various 
organic  diseases  of  the  optic  nerve  or  retina,  such  as  early  optic 
atrophy,  central  retinal  haemorrhage,  &c.,  or  it  may  result,  in  a 
minor  degree,  from  obstruction  to  central  vision,  e.g.  by  central 
opacities  in  the  lens  or  cornea.  It  may  also  occur,  as  a  temporary 
phenomenon,  in  some  cases  of  migraine.  Such  conditions  are  easy 
of  recognition.  Central  colour  scotoma  to  red  and  green  (detected 
in  a  similar  fashion  with  coloured  objects)  together  with  deficient 
visual  acuity,  is  highly  suggestive  of  tobacco  amblyopia.  In  such 
cases,  besides  a  history  of  chronic  excess  in  tobacco,  we  look  for 
corroborative   signs   such  as   fine  tremor  of   the   hands,    cardiac 


132  NERVOUS    DISEASES 

irregularity,  cardiac  pain,  &c.  An  almost  identical  amblyopia  may 
also  occur  from  chronic  alcoholism. 

The  visual  field  may  be  concentrically  contracted.  This  con- 
dition is  sometimes  due  to  optic  atrophy,  the  field  being  reduced 
to  a  small  area  surrounding  the  fixation-point,  so  that  the  patient 
looks  at  the  outer  world  as  though  through  a  narrow  tube.  Con- 
centric contraction  of  the  field  of  vision  for  blue,  sometimes  actually 
amounting  to  blue-blindness,  may  occur  in  cases  of  increased 
intra-cranial  pressure,  especially  from  cerebral  tumours.^  More 
commonly  concentric  contraction  of  the  visual  field  occurs  in 
hysteria,  the  field  on  the  hemiplegic  side  of  the  body  being  more 
contracted  than  that  on  the  other  side  (Fig.  58),  Temporary 
contraction  of  the  visual  field  may  occur  in  myasthenia  gravis. 
Less  frequently  a  cortical  lesion  of  the  angular  gyrus,  not  impli- 
cating the  subjacent  optic  radiation  (Fig.  29),  causes  a  similar 
concentric  contraction  of  both  fields,  more  marked  in  the  eye  of 
the  side  opposite  to  that  of  the  brain  lesion.  This  is  somewhat 
clumsily  named  crossed  amblyopia,  but,  as  previously  observed, 
it  is  much  commoner  in  hysteria  than  in  organic  brain  disease, 
and  in  hysteria  it  is  frequently  associated  with  diminution  or  loss 
of  other  special  senses  on  the  side  of  the  more  contracted  j&eld 
whose  colour  sense  is  frequently  lost  (achromatopsia).  Hysterical 
amblyopia  is  unknown  to  the  patient,  and  is  only  discovered  on 
examination  by  the  physician. 

Hemianopia  (Fig.  59)  means  bhndness  of  half  the  visual  field, 
right  or  left  as  the  case  may  be,  from  causes  other  than  retinal 
disease.  It  usually  afEects  the  visual  field  of  both  eyes,  and  is  due 
to  a  lesion  of  the  visual  fibres  at  or  behind  the  optic  chiasma. 
Such  chiasmatic  lesions  may  result  from  pressure  by  tumours, 
syphihtic  or  inflammatory  affections  of  the  basi-sphenoid,  from 
tumours  of  the  brain  or  of  its  membranes,  and  especially  from 
pituitary  tumours,  as  in  acromegaly.  We  have  already  considered 
the  signs  of  lesions  of  the  optic  tracts,  and  it  is  convenient  here 
to  recall  the  effects  of  lesions  of  the  optic  chiasma. 

(A)  If  the  lesion  be  in  the  central  part  of  the  chiasma,  inter- 
rupting the  decussating  optic  fibres  (belonging  to  the  nasal  halves 
of  both  retinae),  there  is  blindness  in  the  outer  half  of  each 
visual  field  : — bi-temporal  hemianopia  (Fig.  60).  This  sometimes 
occurs  in  pituitary  tumours. 

1  Gushing,  Johns  Hopkins  Hosp.  Bull.,  1909,  xx.  p.  95. 


CRANIAL    NERVES 


133 


(B)  If  the  lesion  be  situated  at  one  or  other  lateral  extremity 
of  the  chiasma,  it  will  interrupt  merely  the  non-decussating  fibres 
of  the  optic  nerve  and  optic  tract  on  that  side,  causing  unilateral 
nasal  hemianopia  in  the  corresponding  eye.  To  produce  bilateral 
nasal  hemianopia  there  must  be  two  separate  lesions,  one  at  each 


/,,/?  /Tj 


Fig.  58. — Crossed  amblyopia,  in  a  case  of  hysteria. 


/iil/he  £y^ 


,80  80; 


Fig.  59. — Eight  homouymous  hemianopia,  in  a  case  of  softening  of  the  left 
occipital  lobe. 

end  of  the  chiasma,  a  condition  which  very  seldom  occurs.  A 
lesion  involving  the  central  part  of  the  chiasma  and  extending  to 
one  or  other  side  (Fig.  60,  A  flus  B)  will  produce  the  sum  of  these 
two,  namely  bi-temporal  hemianopia  flus  unilateral  nasal  hemi- 
anopia, i.e.  total  blindness  of  one  eye  with  temporal  hemianopia 
of  the  other. 


134  NERVOUS   DISEASES 

(C)  A  lesion  of  the  left  optic  tract  behind  the  chiasma  produces, 
as  already  seen,  hemianopia  in  the  right  halves  of  both  fields 
of  vision. 

(D)  A  lesion  of  one  optic  nerve  simply  causes  blindness  in  the 
corresponding  eye. 

In  rare  cases  we  may  have  a  quadrantic  hemianopia  in  which 
only  one  quadrant  (instead  of  one-half)  of  both  visual  fields  is  blind. 
This  is  generally  due  to  a  lesion  limited  to  part  of  the  cortical  half- 
vision  centre  in  the  cuneate  lobule  and  lingual  gyrus.  The  calcarine 
fissure  divides  the  half-vision  centre  into  an  upper  and  a  lower  part. 

R.  Optic  Tract  L.  Optic  Tract. 


R.  Eye.  L.  Eye. 

Fig.  60. — Diagram  of  course  of  visual  fibres  in  optic  chiasma. 
(Hamilton.) 

A  lesion  above  the  calcarine  fissure,  i.e.  in  the  cuneate  lobule, 
causes  blindness  of  the  lower  quadrant,  whilst  a  lesion  below  the 
calcarine  fissure,  i.e.  in  the  lingual  gyrus,  causes  blindness  of  the 
upper  quadrant  of  the  corresponding  half -fields.-^ 

The  optic  discs  and  retinae  should  be  examined  with  the 
ophthalmoscope  in  every  case  of  nervous  disease.  Every  neur- 
ologist must  be  able  to  use  the  ophthalmoscope.  The  most  im- 
portant conditions  to  look  for  are  optic  neuritis  and  optic  atrophy. 
Optic  neuritis  occurs  in  numerous  pathological  conditions  within 
the  skull,  especially  in  intra-cranial  tumours  and  in  tuberculous 
meningitis.     But  it  also  occurs  in  nephritis,  in  lead  poisoning,  in 

^  Henschen,  Le  Centre  cortical  de  la  Vision.  Internat.  Med.  Congress, 
Paris,  1900. 


CRANIAL    NERVES  135 

diabetes,  and  in  severe  anaemia  ;  and  these  four  common  conditions 
must  always  be  excluded  before  we  diagnose  gross  intra-cranial 
disease.  We  may  also  meet  with  optic  neuritis  in  certain  cases  of 
cervical  myelitis.  Optic  atrophy  may  occur  primarily,  as  in  tabes 
and  disseminated  sclerosis,  or  it  may  be  a  secondary  post-neuritic 
process.  Sometimes  it  follows  a  retro-hulhar  neuritis,  which  is  due 
most  frequently  to  the  toxin  of  disseminated  sclerosis,  less  com- 
monly to  chronic  alcohol  or  tobacco  poisoning.  Pallor  of  the 
temporal  halves  of  the  optic  discs  is  often  an  early  sign  of  dissemi- 
nated sclerosis.  The  combination  of  optic  atrophy,  blindness,  and 
mental  deficiency  occurs  in  the  amaurotic  family  idiocy  of  Tay  and 
Sachs,  an  affection  of  certain  Jewish  children,  coming  on  in  infancy. 
In  these  cases,  on  ophthalmoscopic  examination  there  is  a  char- 
acteristic cherry-red  spot  seen  at  the  macula  lutea,  due  to  local 
oedema  and  atrophy  of  the  retina,  whereby  the  vascular  choroid 
shines  through.  Apart  from  optic  neuritis  and  optic  atrophy,  we 
must  be  on  the  look-out  for  other  pathological  conditions  of  the 
fundus,  such  as  choroiditis,  albuminuric  retinitis,  tubercle  of  the 
choroid,  occlusion  of  the  central  retinal  artery,  retinal  haemor- 
rhage, &c. 

It  must  be  remembered  that  a  patient  may  have  severe  optic 
neuritis  without  any  impairment  of  vision.  Optic  atrophy,  on  the 
other  hand,  causes  the  visual  field  to  contract  concentrically  to  a 
greater  or  less  extent,  whilst  the  visual  acuity  diminishes  and 
ultimately  the  eye  becomes  blind.  The  atrophy  of  retro-bulbar 
neuritis  often  produces  central  scotoma  from  affection  of  the  papillo- 
macular  bundle  of  optic  nerve  fibres.  Scotoma  is  often  the  first 
sign  of  retro-bulbar  neuritis,  long  before  atrophy  is  visible  by 
the  ophthalmoscope. 

Third,  Fourth,  and  Sixth  Nerves. — It  is  convenient  to  study 
together  these  three  nerves  which,  between  them,  innervate  all 
the  voluntary  muscles  of  the  eye.  The  distribution  of  each  is  as 
follows  : — The  third  nerve  (oculo-motorius)  suppHes  all  the  external 
ocular  muscles  except  two  : — the  superior  oblique  suppUed  by  the 
fourth  nerve,  and.  the  external  rectus  supplied  by  the  sixth.  It 
also  suppHes  the  voluntary  part  of  the  levator  palpebrse  superioris 
(the  involuntary  part  being  supphed  by  the  cervical  sympathetic), 
and  it  contains  fibres  which  indirectly,  through  the  ciliary  gangHon 
and  short  ciliary  nerves,  supply  the  non- striated  sphincter  pupillse  and 
ciliary  muscle.     The  fourth  nerve  (patheticus)  supplies  the  superior 


136  NERVOUS    DISEASES 

oblique   alone,   the   sixth    nerve    (abducens)   the   external    rectus 
alone. 

Until  comparatively  recently,  the  motor  nucleus  for  the  pupil  was 
generally  considered  to  be  located  exclusively  in  the  third  nucleus,  and 
in  a  special  part  of  it  near  its  anterior  end  (the  so-called  Edinger- 
Westphal  nuclei,  situated  close  to  the  middle  line,  one  on  each  side, 
consisting  of  small  nerve  cells  of  the  cranial  autonomic  system  embedded 
amongst  the  larger  cells  of  the  oculomotor  nucleus).     To  explain  the 
occurrence  of  loss  of  the  light-reflex,  various  theoretical  lesions  were 
assumed,  sometimes  in  these  Edinger-Westphal  nuclei  (Bernheimer  ^), 
sometimes  in  Meynert's  fibres  leading  from  the  anterior  corpora  quadri- 
gemina  to  the  supposed  pupillary  centre  in  the  third  nucleus.     But 
cases  have  been  recorded  of  tumour  of  the  mid-brain,  completely  de- 
stroying the   oculomotor  nuclei  and   so   producing   ophthalmoplegia 
externa,  and  yet  the  pupillary  reflex,  still  remained  (Biancone,^  Jacob- 
sen  3).    Moreover,  total  ophthalmoplegia,  internal  and  external,  has 
occurred    without    any    affection    of    the    Edinger-Westphal    nuclei 
(Monakow^).     Further,  degeneration  of  Meynert's  fibres  has  not  been 
demonstrated,  even  in  cases  of  tabes  or  general  paralysis  where  loss 
of  the  pupillary  light-reflex  is  one  of  the  commonest  clinical  phenomena. 
Lastly,  experimental  and  clinical  evidence  (Piltz,^  Bach^)  has  shown 
that  the  ciliary  ganglion  of  the  cranial  autonomic  system  is  the  peri- 
pheral motor  nucleus  controlling  the  sphincter  pupillse,  and  Marina,'^ 
in  a  series  of  twenty-eight  cases  of  tabes  and  general  paralysis  exhi- 
biting the  Argyll-Robertson  pupil,  found  this  ganglion  invariably  de- 
generated.   In  one  of  them  where  the  Argyll-Robertson  phenomenon 
was  confined  to  one  eye,  the  ciliary  ganglion  was  degenerated  on  that 
side  alone,  the  ganglion  of  the  other  side  being  normal.     It  is  therefore 
probable  that  degeneration  renders  the  ciliary  ganglion  inexcitable 
to  the  stimulus  of  light,  whereas  it  can  still  respond  to  the  stronger 
stimulus   of  voluntary  impulses  transmitted  along  the  third  nerve. 
The  connection  between  the  anterior  corpus  quadrigeminum  and  the 
third  nerves  is  vid  the  fasciculus  sublongitudinalis.^ 

The  Pupil. — We  note  the  size  of  the  pupil,  both  in  a  bright 
and  in  a  dim  light.  Firstly,  we  observe  whether  the  pupils  are 
equal  in  diameter.  Slight  inequality  {anisocoria)  of  the  pupils  is 
not  uncommon  in  individuals  who  are  otherwise  healthy,  and  if 
the  pupils  react  to  Hght  and  to  convergence,  such  trivial  inequality, 
by  itseU,  has  no  special  significance.  Marked  inequality,  how- 
ever,   should    always    make   us    suspicious    of    organic   mischief. 

1  V.  Graefe's  Archiv,  1897.  ^  Rivista  di  Freniatria,  1899. 

^  Deutsche  Med.  Wochensch.,  1900. 

*  Gehirn-pathologie,  4te  Aufl.  1905,  s.  1053. 

5  Neurologisches  Gentralblatt,  1903.  ®  Zeitsch.  fur  Augenheilkunde,  1904. 

'  Annali  di  Nevrologia,  1901. 

*  Majano,  MoTiatschrift  fur  Psychiatrie  und  Neurologie,  1903,  Bd.  xiii.  Heft  1. 


CRANIAL    NERVES  137 

Abnormal  dilatation  of  the  pupils  {mydriasis)  is  often  present 
in  anaemia  and  neurasthenia,  but  it  may  occur,  on  one  or  both 
sides,  in  organic  nervous  disease.  Mydriasis  may  be  either  para- 
lytic, ^from  paralysis  of  the  sphincter  pupillse,  as  in  disease  of 
the  third  nerve  or  ciliary  ganglion,  or  it  may  be  irritative,  as 
when  due  to  stimulation  of  the  dilator  pupillse.  It  also  occurs 
when  optic  atrophy  has  caused  blindness,  and  is  then  due  to  the 
absence  of  visual  impressions.  Myosis  or  abnormal  contraction  of 
the  pupils  occurs  in  pontine  haemorrhage,  probably  from  irritation 
of  inhibitory  fibres  leading  from  the  brain  to  the  ciliary  ganglia.^ 
It  is  also  present  in  many  cases  of  tabes,  as  well  as  in  certain 
cases  of  disease  of  the  cervical  region  of  the  cord  (notably  in 
syringomyelia)  from  interruption  of  the  pupil-dilating  fibres.'^ 
Myosis  is  also  caused  by  iritis  and  by  the  irritation  of  foreign 
bodies  in  the  cornea,  and  a  transient  myosis  occurs  for  a  day  or 
so  after  excision  of  the  Gasserian  ganglion  ^  (see  Fig.  61). 

Variations  in  the  size  of  the  pupil  may  also  be  the  result  of 
mydriatic  drugs,  either  locally  instilled  (atropine,  homatropine, 
cocaine)  or  taken  internally  (belladonna),  whilst  other  drugs  are 
myotics,  either  local  (eserine,  pilocarpine)  or  internal  (opium, 
jaborandi). 

The  outline  of  the  pupil  should  be  carefully  examined.  Some- 
times, instead  of  being  circular,  it  is  oval  or  irregularly  polygonal. 
Such  variations  have  an  important  diagnostic  value.  For  if  we 
exclude  congenital  malformation  such  as  coloboma,  operative  pro- 
cedures such  as  iridectomy,  and  disease  such  as  iritis  causing 
synechise,  then  it  may  be  taken  as  a  general  rule  that  irregularity  of 
the  pupils  signifies  either  tabes,  general  paralysis,  or  old  syphiUs, 
the  lesion  being  either  in  the  short  cihary  nerves  or  in  the  ciUary 
ganglion  itself.  Ectopia  pupillcB  is  a  condition  in  which  the  pupil 
is  not  in  the  centre  of  the  iris.  Sometimes  it  occurs  in  lesions 
of  the  mid -brain ;  *  in  other  cases,  however,  it  appears  to  have 
no  pathological  significance.  Irregularity  of  the  pupil  can  be  pro- 
duced experimentally  by  stimulation  or  division  of  the  short 
ciliary  nerves. 

The  pupillary  reflex  to  light  should  always  be  observed.  For 
this  purpose  it  is  convenient  to  have  the  patient  sitting  near 

^  Bach,  Zeitschrift  filr  Augenheilkunde,  1904,  s.  105. 

2  See  later,  Cervical  Sympathetic, p.  366.       ^  H.  M.  Dsbvies,  Brain,  1907,  p.  265. 

4  S.  A.  K.  Wilson,  Brain,  1906,  p.  524. 


138 


NEEVOUS    DISEASES 


a  window  in  sucli  a  position  that  one  side  of  his  face  is  illuminated. 
He  is  then  made  to  gaze  at  the  ceiling  whilst  the  physician,  with 
the  palms  of  the  hands,  shades  and  uncovers  one  or  both  eyes. 
Each  eye  must  be  observed  separately,  noting  the  effect  on  the 
pupil  of  shading  and  uncovering,  first  the  same  eye  and  then  the 
opposite  eye.  Normally  the  iris  contracts  when  Hght  falls  on  the 
retina,  whether  of  the  same  eye  (direct  reflex)  or  of  the  opposite 
eye  (consensual  reflex).  The  light-reflex  depends  upon  the  integrity 
of  a  reflex  arc,  whose  aflerent  limb  is  the  peri-macular  fibres  of  the 


Corporob  Qiwuirigemijuxj 


Efferent,  i, 

Mixbitory  Fibres  franv 
Braiwto  CiJbuxjyGangTion 


HI  Nucleus 


(^  Ciliary  GajicfLionj. 

PupiL  constriclxTigl'ibres. 


R.EYB 


Jj  .EYE 


CervtcaZSympcUJiettc 
Fig.  61. — Diagram  of  the  path  of  the  pupil-reflex  (modified  from  Bach). 

retina  and  optic  nerve,  whose  intermediate  station  is  in  the  mid- 
brain, and  whose  efferent  limb  passes  through  the  third  nerve  and 
ciliary  ganglion  to  the  pupillary  sphincter  (Fig.  61). 

If  the  healthy  pupil  be  strongly  illuminated  and  examined  with 
a  magnifying  lens  (say  x  10),  we  observe  that  it  is  not  stationary 
but  in  a  continuous  state  of  fine  irregular  movement,  slight 
alternate  narrowing  and  widening,  varying  both  in  rhythm  and 
amplitude.  This  normal  pupillary  unrest  ^  must  not  be  confounded 
with  hippus,  which  is  a  pathological  condition  consisting  in  rhythmic 
clonic  contractions  of  the  iris,  regular  in  their  periodicity,  much 
coarser  in  range,  and  visible  to  the  naked  eye.     Loss  of  the  normal 

1  Hiibner,  Archiv  fiir  Psychiatric,  1906,  Band  41,  s.  1016. 


CRANIAL    NERVES  139 

pupillary  unrest  is  always  pathological,  and  may  be  one  of  the 
earliest  signs  of  organic  affection  of  the  reflex  visual  path,  e.g.  in 
tabes  or  general  paralysis. 

Loss  of  reaction  to  light  occurs  in  optic  atrophy,  in  paralysis 
of  the  third  nerve,  and  in  degeneration  of  the  ciliary  ganglion. 
Loss  of  the  light-reflex  with  preservation  of  contraction  during 
accommodation  for  near  objects — ^the  classic  Argyll  -  Robertson 
phenomenon — occurs  typically  in  tabes  and  in  general  paralysis 
of  the  insane.  It  also  occurs  sometimes  in  cerebro-spinal  syphilis 
apart  from  tabes  or  general  paralysis,  and  it  has  been  demonstrated 
in  a  few  rare  cases  without  syphihtic  infection,  e.g.  in  chronic 
alcohoHsm  ^  and  even  in  syringomyeha.^  Marina  has  shown  it  to 
be  associated  with  degeneration  of  the  ciUary  ganghon.  It  also 
occurs  in  bhndness  from  optic  atrophy. 

In  the  early  stages  of  optic  atrophy  the  pupil  of  the  affected 
eye  may  contract  to  light  fairly  well  for  a  moment,  but  under 
continued  exposure  it  dilates  again,  unlike  a  healthy  pupil.^  If 
this  phenomenon  be  associated  with  diminution  of  visual  acuity 
or  with  failure  to  distinguish  between  red  and  green  in  the  centre 
of  the  visual  field,  we  should  be  suspicious  of  early  optic  atrophy 
(even  though  the  optic  disc  be  normal  in  appearance),  which  in 
many  cases  is  due  to  commencing  disseminated  sclerosis.  Wernicke's 
hemiopic  pupillary  reaction,  in  certain  cases  of  hemianopia,  is 
absence  of  pupillary  contraction  when  a  ray  of  light  is  thrown  on 
the  blind  side  of  the  retina.  It  signifies  a  lesion  of  the  visual  path 
behind  the  chiasma,  and  below  or  at  the  corpora  quadrigemina. 
In  retro-quadrigeminal  hemianopia,  where  the  lesion  is  anywhere 
between  the  corpora  quadrigemina  and  the  visual  cortex,  the 
pupillary  reaction  is  normal  (Fig.  29,  p.  46). 

The  reaction  of  the  pupil  to  accommodation  is  the  contraction  of 
the  pupil  which  occurs  when  the  patient  converges  the  eyes  to  look 
at  a  near  object.  We  test  this  by  holding  a  finger  close  to  the 
patient's  face,  first  telling  him  to  look  at  some  distant  object, 
and  then  suddenly  to  look  at  the  finger.  If  he  is  bhnd,  he 
can  nevertheless  converge  by  attempting  to  look  at  his  own  finger. 
In  paralysis  of  the  third  nerve  there  is  total  immobility  of  the 
corresponding  pupil,  both  to  fight  and  on  convergence.    Loss  of  the 

1  Noune,  N eurologisches  Centralblatt,  1912,  p.  5. 

^  Sicard  and  Galezowski,  Revue  neurologique,  1914,  p.  300. 

3  Gunn,  Brit.  Med.  Journal,  1907,  p.  353. 


140 


NERVOUS    DISEASES 


contraction  on  accommodation  with  preservation  of  the  light-reflex 
— a  condition  the  converse  of  the  Argyll-Robertson  phenomenon 
— is  not  uncommon  after  diphtheria,  and  is  often  accompanied 
by  other  evidences  of  post-diphtheritic  nem:itis,  such  as  paralysis 
of  external  ocular  muscles  or  of  the  palate,  loss  of  knee-jerks, 
&c.  Paradoxical  pupillary  reaction  is  when  the  pupil  dilates 
mstead  of  contracting  on  accommodation.  This  phenomenon, 
which  is  not  uncommon  in  tabes  (occurring,  according  to  Pilcz,  in 
40  per  cent,  of  cases),  can  be  demonstrated  in  two  ways.  Firstly, 
energetic  voluntary  closure  of  the  eye  .produces  a  synergic  con- 


JnHO 


SupJt 


Sup.R 


Inf.O 


bubR.     IntH. 


Sup.O.  Inf.R.  InT.R.  Sup.O. 

Fig.  62. — N.  Bishop  Harman's  chart  to  show  (1)  Movonents  of  ocular  muscles, 
and  (2)  Position  of  false  image  in  paralysis. 

1  (a)  Rectangular  movements.  The  arrows  point  to  the  direction  in  which  the  eye  is  turned 
by  each  muscle. 
(6)  Rotation.  Put  a  match,  head  upwards,  on  each  of  the  dotted  lines  indicating  the 
vertical  meridians.  Muscles  that  rotate  eye  inwards  turn  the  match-head  towards 
nose  (Sup.  Rectus  and  Sup.  Oblique) ;  those  that  rotate  it  outwards  turn  match  in  the 
opposite  direction  (Inf.  Oblique  and  Inf.  Rectus). 

2.  Put  matches  on  diagram  again.  The  match  will  represent  the  true  image.  The  four  rays 
marked  Sup.  R.,  Inf.  R.,  Sup.  0.,  and  Inf.  O.  will  represent  the  relative  position  (in 
vertical  and  lateral  displacement  and  tilting)  of  the  false  image  produced  in  paralysis 
of  each  of  these  muscles.  In  paralysis  of  Int.  or  Ext.  Rectus  the  false  image  will  run 
vertically  through  the  corresponding  arrow-head. 

traction  of  the  pupil,  which,  when  the  eye  is  re-exposed  to  light, 
dilates  again.  Secondly,  if  we  tell  the  patient  to  depress  the 
upper  hd  whilst  we  forcibly  prevent  it  from  descending,  we  see 
the  pupil  contract,  whilst  the  eye  moves  upwards  and  out- 
wards to  get  under  cover  of  the  upper  lid. 

The  reaction  of  the  pupil  to  painful  stimulation  of  ^the  skin  of 
the  neck,  causing  the  pupil  to  dilate,  is  important  with  regard  to 
the  cervical  sympathetic.  It  is  often  absent  in  the  early  stages 
of  tabes.  A  psychical  dilatation  of  the  pupil  also  occurs,  tempor- 
arily, mider  the  influence  of  lively  emotion,  such  as  fear,  intense 
interest,  sexual  orgasm,  &c.  The  pupil  may  even  contract  or  dilate 
when  the  individual  thinks  of  a  dark  object  or  a  luminous  one. 

Let  us  now  consider  paralysis  of  external  ocular  muscles. 


CRANIAL    NERVES 


141 


To  detect  paralysis  of  the  ocular  muscles,  having  first  examined 
the  pupils,  noting  their  size  and  any  irregularity  of  outline,  and 
having  tested  their  reaction  to  light  and  on  accommodation,  we 
then  ask  the  patient  to  follow  our  finger  with  his  eye,  making  him 
look  alternately  up,  down,  to  the  right  and  left,  and  finally  making 
him  converge.  Meanwhile  we  observe  whether  there  be  any  squint, 
deficient  movement  in  any  direction,  diplopia,  or  nystagmus. 

If  an  individual  muscle  be  paralysed,  there  is  diplopia,  squint, 
and  deficiency  of  movement  of  the  affected  eye  towards  the  direc- 
tion of  traction  of  the  affected  muscle.     Fig.  62  is  Bishop  Harman's 


Left    supr. 
Rectus 


Right    supr. 
RectuA 


Left  infr. 
Rectus 


Right  infr. 
Rectus 


Left  infr.- 
oblique 


Right  infr. 
oblique 


Left  supr. 

oblique    - 


Right  supr. 
oblique 


Fig.  63. 


Fig.  64. 


Figs.  63  and  64. — Werner's  "artificial  memory  "  for  the  double  images  in  ocular 
paralyses  {Ophthalmic  Eevieiv,  1886).  Fig.  63  shows  the  position  of  the 
images  in  paralysis  of  the  recti  muscles.  Fig.  64  in  paralysis  of  the  oblique 
muscles.  The  dotted  lines  indicate  "false"'  images,  the  thick  black  lines 
"  true  "  images. 

diagram  indicating  the  action  of  the  individual  muscles.  A  simple 
rule,  worth  remembering  in  all  cases  of  ocular  paralysis,  is  that  the 
affected  eye  is  displaced  (by  the  unopposed  antagonists)  in  a  direction 
opposite  to  the  direction  of  traction  of  the  paralysed  muscle,  whilst 
the  false  image,  seen  by  the  affected  eye,  is  displaced  in  the  direction 
of  traction  of  the  paralysed  muscle.  Figs.  63  and  64  are  Werner's 
well-known  "  memoria  technica,"  showing  the  position  of  the  false 
image  in  the  various  ocular  paralyses.  Fig.  63  shows  the  position 
of  the  false  image  in  paralysis  of  any  of  the  recti ;  Fig.  64  in 
paralysis  of  the  oblique  muscles.  For  example,  Fig.  63  shows 
that    in    diplopia    from    paralysis    of    the    left    inferior    rectus, 

(1)  the  false  image  is  on  the  right  of  the  true  {i.e.  it  is  crossed) ; 

(2)  the  false  image  has  its  upper  end  inclined  towards  the  true ; 


142  NEKVOUS    DISEASES 

(3)  the  false  image  is  lower  than  the  true ;  and  (4)  the  diplopia 
occurs  on  downward  movement  of  the  eyes.  To  test  diplopia  we 
use  a  long,  lighted  candle,  at  a  distance  of  about  three  yards  from 
the  patient,  holding  it,  first,  exactly  opposite  the  patient  and 
moving  it  gradually  from  side  to  side  and  then  from  above  down- 
wards. One  of  the  patient's  eyes  is  covered  with  a  red  and  the 
other  with  a  green  glass,  to  differentiate  the  two  images,  and  the 
patient  has  to  tell  us  the  relative  position  of  the  red  and  of  the 
green  candle.  It  is  necessary  to  ensure  that  the  patient  keeps 
his  head  fixed  during  the  process  of  testing.  The  false  image  is 
that  seen  by  the  paralysed  eye,  the  true  image  by  the  sound  one. 

Diplopia  is  a  more  dehcate  test  than  paralytic  squint,  for  where 
there  is  shght  paresis  of  an  ocular  muscle  there  may  be  no  notice- 
able squint,  and  yet  the  diplopia  may  be  quite  appreciable  to  the 
patient.  To  detect  a  paralytic  squint  we  direct  the  patient  to  follow 
our  finger,  moving  it  laterally  from  side  to  side,  and  then  vertically 
up  and  down,  and  observe  whether  there  is  deficiency  of  movement 
of  one  or  both  eyes  in  any  particular  direction  or  directions. 

Nystagmus  is  an  involuntary  rhythmic  tremor  of  the  eyeballs, 
generally  bilateral  and  symmetrical.  The  movement  consists  of 
an  oscillation,  usually  horizontal,  from  side  to  side,  but  sometimes 
vertical  or  even  rotatory,  or  it  may  be  circumductory — a  combina- 
tion of  rotation  with  vertical  and  horizontal  movements.  Nystag- 
mus may  be  either  pendular  (where  the  movements  to  both  sides 
are  equal  in  range  and  of  equal  speed)  or  rhythmic,  the  commoner 
type,  where  both  movements  are  equal  in  range  but  the  one  is 
a  fast  jerk  and  the  other  a  slow  one.  In  most  cases  nystagmus 
occurs  only  when  the  eyes  are  voluntarily,  moved  to  an  extreme 
degree  either  laterally  or,  less  commonly,  vertically  ;  in  rhythmic 
horizontal  nystagmus  the  rapid  jerk  is  to  the  side  towards  which 
the  eyes  are  directed.  But  sometimes,  especially  in  the  rotatory 
variety,  nystagmus  occurs  when  the  eyes  are  directed  straight 
forward.  In  cases  in  which  an  ocular  muscle  has  been  paralysed 
but  is  in  process  of  recovery,  if  we  make  the  patient  look  steadily 
in  a  direction  which  necessitates  the  active  movement  of  the  paresed 
muscle,  shght  rhythmic  nystagmus  may  develop,  analogous  to 
tremulousness  of  the  hand  after  carrying  a  heavy  weight. 

Another  variety  is  lahyrinthine  or  vestibular  nystagmus.  This,  to- 
gether with  violent  vertigo,  may  be  produced  experimentally  in 
healthy  subjects  by  syringing  the  drum  of  the  ear  with  water,  either 


CRANIAL   NERVES  143 

distinctly  above  or  distinctly  below  the  temperature  of  the  body. 
Bfclrany  ^  regards  this  nystagmus  as  a  result  of  convection  currents 
in  the  endolymph  produced  by  warming  or  cooling  of  the  labyrinth. 
The  presence  of  such  thermic  nystagmus  can  be  used  as  a  test  of 
the  integrity  of  the  vestibular  nerve.  The  objective  phenomena 
vary  according  to  the  position  of  the  patient's  head.  Thus,  for 
example,  if  the  patient  be  standing  up,  with  the  head  turned 
face  downwards,  and  if  the  left  ear  be  irrigated  with  cold  water, 
the  nystagmus  which  is  produced  is  horizontal  in  type  with  the 
quick  jerk  to  the  left  and  most  marked  when  the  patient  looks 
towards  the  left  side.  Meanwhile  the  head  and  eyes,  and  also 
the  trunk,  tend  to  rotate  strongly,  around  the  long  axis  of  the 
body,  towards  the  right  side.  If  the  patient's  head  be  erect  when 
his  left  ear  is  syringed  with  cold  water,  the  nystagmus  is  rotatory 
in  type  and  to  the  right,  and  the  forced  movement  of  the  head  and 
trunk  is  a  lateral  bending  towards  the  left  side.  If  the  patient 
lies  on  his  back,  when  the  left  ear  is  irrigated  with  cold  water,  he 
will  tend  to  roll  towards  the  ipso -lateral  side  and  horizontal 
rhythmic  nystagmus  will  be  noticed  towards  the  contra-lateral  side. 
If  hot  water  be  used  instead  of  cold,  the  direction  of  nystagmus 
and  of  forced  movement  of  the  head,  eyes,  and  trunk  is  in  each 
case  reversed.^ 

In  some  cases  of  otitis  media,  in  which  a  fistulous  communication 
exists  between  the  middle  ear  and  the  internal  ear,  sudden  raising 
of  the  pressure  in  the  middle  ear,  e.g.  by  compressing  the  external 
auditory  meatus  with  the  finger,  or  by  inflation  of  the  ear  through 
the  external  meatus,  stimulates  the  external  semicircular  canal 
through  the  fistulous  opening  and  produces  sudden  labyrinthine 
nystagmus  and  vertigo,  in  which  the  nystagmus  is  horizontal  in  type, 
the  head  and  eyes  being  deviated  towards  the  contra-lateral  side. 
If  the  labyrinth  be  already  destroyed  this  fistular  test  is  negative. 

In  cases  of  labyrinthitis,  e.g.  by  inward  spread  from  an  otitis 
media,  there  is  total  deafness  of  the  affected  side,  together  with 
complete  loss  of  thermic  and  of  fistular  nystagmus.  The  inflamed 
labyrinth  produces  spontaneous  vertigo  with  nausea,  vomiting, 
and  with  a  spontaneous  rotatory  nystagmus  towards  the  sound 
side,  if  the  head  be  in  the  erect  posture. 

Nystagmus  occurs  in  various  central  organic  diseases,  not  of 

'  Gentralhlatt  fiir  Augenheilkunde,  August  1905. 
*  Scott,  Lancet,  June  11,  1910. 


144  NERVOUS    DISEASES 

the  cerebral  hemispheres,  but  of  the  mid-brain,  pons,  and  cere- 
beUiim.  It  is  specially  characteristic  of  disseminated  sclerosis, 
Friedreich's  ataxia,  cerebellar  disease,  and  syringomyelia.  It 
may  also  occur  in  alcoholic  peripheral  neuritis.  It  is  present 
also  in  certain  patients  who  have  become  more  or  less  blind 
(though  in  complete  blindness  the  movement  is  more  often 
a  slow,  aimless  rolling  of  the  eyes),  also  in  albinism  (where  the 
vision  is  congenitally  impaired),  and  a  well-recognised  form  is 
miner's  nystagmus,  due  to  persistent  ocular  strain  in  a  dim  light. 
Miner's  nystagmus  is  pendular  but  very  fine  and  rapid,  generally 
vertical,  worse  on  looking  upwards,  and  accompanied  by  spasm  of 
the  levator  palpebree.     It  is  often  associated  with  vertigo. 

Labyrinthine  nystagmus  can  also  be  producedin  a  normal  person  by  j)lacing 
him  on  a  rotating  stool  with  the  head  erect  and  spinning  him  rapidly  around 
the  long  axis  of  his  own  body ;  in  snch  a  case,  if  the  stool  be  suddenly 
stopped,  the  endolymph  keeps  on  moving  for  a  time  and  a  temporary  after- 
nystagmus  appears,  horizontal  and  rhythmic,  the  rapid  phase  of  the  nystag- 
mus being  in  the  opposite  direction  from  the  previous  rotation.  If  a 
patient  who  already  has  a  horizontal  nystagmus  be  similarly  revolved 
around  his  own  long  axis,  on  suddenly  stopping  the  rotation  we  find  that  the 
original  nystagmus  towards  the  direction  of  rotation  has  temporarily  ceased 
whilst  that  in  the  opposite  direction  is  exaggerated.^  In  such  a  case,  the 
experimental  after-nystagmus  lias  for  the  time  over-compensated  the  pre- 
existing nystagmus. 

There  is  also  a  rare  congenital  affection  known  as  nystagmus- 
myoclonus,  in  which,  together  with  nystagmus,  commonly  of  the 
lateral  pendular  variety,  there  are  involuntary  jerking  movements 
of  the  limbs  or  trunk.  These  movements  are  aggravated  by  cold  or 
by  tapping  the  muscles,  but  can  be  controlled  by  an  effort  of  will. 
The  deep  reflexes  are  often  exaggerated,  and  it  is  not  unusual  to 
have  other  co-existing  deformities,  such  as  hypospadias,  flat-foot, 
facial  asymmetry,  persistent  branchial  cleft,  &c.^ 

We  are  now  in  a  position  to  recognise  the  signs  of  paralysis 
of  any  of  the  ocular  nerves.  In  a  case  of  complete  third  nerve 
paralysis  (Figs.  65  and  66)  there  is  ptosis  or  drooping  of  the  upper 
lid,  from  paralysis  of  the  levator  palpebrae,  with  over-action 
of  the  frontalis  on  that  side,  so  that  the  eyebrow  stands  higher 
than  normal.  In  hysterical  ptosis  (Fig.  67),  on  the  other  hand, 
there  is  no  over-action  of  the  frontalis,  nor  is  there  in  the  ptosis  of 
myasthenia  gravis,  since  the  frontalis  is  usually  partially  paralysed 

^  Cassirer  and  Loeser,  Neurologisches  Centralhlatt,  1908,  s.  252. 
^  Lenoble  and  Aubineau,  Revue  de  Medecine,  July  16,  1906. 


CRANIAL    NERVES 


145 


as  well.  In  third  nerve  paralysis  there  is  also  external  strabismus 
from  unopposed  action  of  the  external  rectus,  and  there  is  inabiUty 
to  move  the  eye  upwards,  directly  downwards,  or  directly  inwards, 
although  a  slight  downward  and  inward  movement  can  be  executed 
by  the  superior  oblique.  The  pupil  is  dilated  owing  to  paralysis  of  the 
sphincter  iridis,  and  does  not  contract  either  to  light  or  on  attempted 
accommodation.  Complete  paralysis  of  the  third  nerve  is  less 
common  than  is  a  partial  paralysis  affecting  one  or  more  muscles. 


i'lG.  65. 


Fig.  (16. 


Fig.  65. — Total  paralysis  of  right  third  nerve  from  syphilitic  disease. 
Fig.  66. — The  same  patient,  the  right  eyelid  being  passively  lifted  to  show  the 
external  strabismus  and  dilatation  of  pupil  on  the  jjaralysed  side. 

In  some  cases  of  partial  third  nerve  paralysis  in  which  there  exists 
a  unilateral  ptosis  with  complete  inabihty  to  raise  the  hd  volun- 
tarily, we  observe  that  an  involuntary  elevation  of  the  paralysed 
lid  occurs  if  the  healthy  eye  be  passively  closed  with  the  finger. 
When  the  opposite  eye  is  again  opened,  the  paralysed  lid  drops 
at  once,  with  a  see-saw  movement  {piosi  a  hilancia).  The  explana- 
tion of  this  curious  phenomenon,  which  only  occurs  in  a  certain 
proportion  of  cases,  is  that  the  motor  fibres  to  the  levator  palpebrse 
are  derived  from  the  nuclei  of  both  third  nerves,  and  if  the  crossed 
fibres  of  origin  happen  to  escape,  the  see- saw  phenomenon  can  be 
demonstrated.^ 

^  Paccetti,  Policlinico,  1896,  sez.  med.  fasc.  3. 


146 


NERVOUS   DISEASES 


Weakness  of  tlie  internal  recti  sometimes  occurs  in  exoph- 
thalmic goitre  (constituting  Moebius's  sign).  We  make  the  patient 
look  upwards  to  the  ceihng  and  then  ask  him  to  look  at  the  tip 
of  his  own  nose,  when  we  observe  that  only  one  eye  converges, 
the  other  eye  becoming  divergent. 


Fig.  67. — Case  of  left-sided  hysterical  ptosis  in  a  woman  of  25,  showing 
absence  of  frontalis  over-action  on  paralysed  side.  The  area  on  the  left 
side  of  the  head,  neck,  trunk  and  shoulder,  within  the  black  line,  was 
totally  anjESthetic  to  all  forms  of  stimuli.  Thei'e  was  loss  of  smell  and  taste 
on  the  left  side  :  contraction  of  the  left  visual  field  and  diminution  of 
hearing  in  the  left  ear.  The  figure  also  shows  the  presence  of  "dermo- 
graphism." The  patient's  name  having  been  traced  on  the  chest  with  the 
head  of  a  pin,  a  hard,  cord-like  pattern  was  produced,  capable  of  being 
photographed . 

Paralysis  of  the  Fourth  Nerve  produces  paralysis  of  the 
superior  oblique  muscle  of  the  corresponding  eye.  This  muscle 
has  a  threefold  action  :  it  turns  the  anterior  pole  of  the  eye 
downwards  and  outwards  and  at  the  same  time  rotates  its  vertical 
meridian  slightly  inwards  (see  Fig.  62).      The  deficiency  of  move- 


CRANIAL   NERVES 


147 


merit  is  diflficult  to  see,  and  the  paralysis  is  recognised  mainly 
by  the  characteristic  diplopia  which  occurs  when  the  patient  gazes 
in  the  direction  in  which  the  superior  oblique  ought  to  come 
into  action,  i.e.  downwards  and  outwards.  When  the  patient  looks 
horizontally  forwards  or  upwards  there  is  no  diplopia.  But  when  he 
looks  downwards  and  outwards,  diplopia  appears,  the  false  image 
standing  lower  than  the  true,  and  having  its  upper  end  tilted 
towards  the  other  (Fig.  64).  The  false  image  also  appears  to  the 
patient  nearer  to  him  than  the  true,  the  reason  for  which  is  obscure. 
Moreover  the  patient  feels  giddy,  especially  when  he  looks  down- 


FlG.LGS.  Frc.  C8A. 

Case  of  paralj'sis  of  the  left  sixth  nerve. 

Fig.  68  shows  the  normal  movement  of  both  eyes  on  looking  to  the  right. 
Fig.  68a  shows  attempted  movement  of  eyes  to  the  left.      The  left  eye 
sticks  at  the  mid-position. 

wards,  as  in  walking  downstairs,  and  he  habitually  incKnes  his 
head  forward  and  towards  the  sound  side. 

Paralysis  of  the  Sixth  Nerve  is  particularly  easy  to  recognise. 
There  is  merely  paralysis  of  the  external  rectus,  with  inability  to 
turn  the  eye  outwards  beyond  the  mid-point,  all  other  movements 
being  normal  (Figs.  68  and  68a),  and  there  is  diplopia  on 
looking  outwards.  In  old  cases  in  which  contraction  of  the  non- 
paralysed  internal  rectus  has  supervened,  an  internal  strabismus 
results. 

Sometimes  an  external  ocular  muscle  is  attacked  by  rheumatic 
myositis,  which  causes  an  ocular  palsy  of  benign  form.  The  muscle 
most  frequently  thus  afiected  is  the  external  rectus. 

Ocular  paralyses  differ  in  type  according  as  they  are  due  to 
a  supra-nuclear  lesion  (between  the  second  frontal  gyrus  and  the 


148  NERVOUS    DISEASES 

ocular  nuclei),  a  nuclear  lesion  in  the  mid-brain,  or  an  infra-nuclear 
lesion  of  the  individual  nerves  such  as  we  have  just  described. 

Ocular  paralysis  from  a  supra-nuclear  lesion  never  attacks  a 
single  ocular  muscle  or  even  a  single  eye.  On  the  contrary,  associ- 
ated muscles  of  both  eyes  are  affected.  The  common  type  of 
paralysis  from  a  destructive  lesion  at  or  above  the  internal  capsule 
is  one  in  which  the  patient  loses  the  power  of  turning  both  eyes 
towards  the  contra -lateral  side.  Therefore  the  unopposed  anta- 
gonists draw  both  eyes  over  towards  the  side  of  the  lesion ;  this  is 
called  conjugate  deviation.  In  certain  cases  of  conjugate  deviation, 
although  the  patient  can  no  longer  turn  his  eyes  voluntarily  to 
one  side,  say  the  right,  he  can  do  so  reflexly  by  fixing  some  object 
directly  in  front  with  his  eyes,  this  object  being  then  moved  to- 
wards the  right  or  the  patient's  head  being  passively  rotated  to 
the  left.^  Curiously  enough,  conjugate  deviation  upwards  or 
downwards  does  not  occur  from  a  paralytic  lesion  of  the  internal 
capsule,  unless  a  bilateral  lesion  be  present.  In  supra-nuclear 
lesions  reflex  nystagmus  is  still  preserved.  Barany  ^  has  shown  that 
reflex  nystagmus  can  be  produced  in  normal  individuals  in  two 
ways.  Firstly,  there  is  optic  nystagmus,  produced  by  making  the 
patient  watch  a  rapidly- moving  landscape  when  looking  out  of  the 
window  of  a  railway  carriage,  or  by  making  him  watch  a  series  of 
vertical  bars  on  a  horizontally  revolving  cylinder.  Secondly,  there 
is  vestibular  nystagmus,  produced  either  by  rapid  rotation  of  the 
individual  on  a  revolving  chair  (rotation  to  the  right  producing 
horizontal  nystagmus  to  the  left  and  vice  versd),  or  by  syringing 
the  ear  with  cold  water,  stimulation  of  the  right  ear  producing 
nystagmus,  partly  horizontal  but  mainly  rotatory,  to  the  left  and 
vice  versd  (see  above,  p.  143).  If  the  vestibular  nerve  be  diseased, 
reflex  vestibular  nystagmus  is  abolished.^ 

Skew  deviation  of  the  eyes  occurs  in  certain  lesions  of  the 
lateral  lobe  of  the  cerebellum  or  of  its  middle  peduncle.  Thus  in 
a  woman  with  a  fatal  haemorrhage  in  the  right  half  of  the  cere- 
bellum and  pons,  the  right  eye  was  directed  downwards  and 
inwards,  and  the  left  eye  upwards  and  outwards. 

A  nuclear  lesion  of  the  third,  fourth,  or  sixth  nuclei  in  the  floor 
of  the  Sylvian  aqueduct  may  be  partial  or  complete,  and  the  type 
of   ocular   palsy  which  results  is  called  nuclear  ophthalmoplegia. 

1  Bielschowsky,  Miinchener  medizinische  Wochenschrift,  1903,  s.  1666. 

2  Barany,  ibid.,  1907,  s.  1072. 


CRANIAL   NERVES  149 

In  some  cases  the  fibres  for  the  ciliary  gangUa  or  the  gangha  them- 
selves or  short  ciliary  nerves  to  the  internal  ocular  muscles  (iris 
and  ciliary  muscle)  are  alone  affected,  and  not  the  external  muscles 
of  the  globe.  The  result  is  ophthalmojdegia  interna,  in  which  the 
pupils  are  dilated  and  immobile  both  to  light  and  on  convergence. 
This  condition  may  be  unilateral  or  bilateral,  according  as  the  ciliary 
ganglia  or  short  cihary  nerves  are  affected  on  one  or  both  sides. 
It  often  occurs  as  a  transient  result  of  post-diphtheritic  neuritis. 
Ophthalmo'plegia  externa  is  a  nuclear  disease  of  the  Sylvian  aqueduct 
affecting  numerous  external  ocular  muscles,  generally  of  both  eyes 
and  often  symmetrically.  A  fairly  common  type  is  where  the 
power  of  upward  rotation  of  the  eyes  is  lost,  lateral  movements 
being  still  possible.  Ophthalmoplegia  externa  usually  occurs  alone, 
less  commonly  it  is  associated  with  the  internal  variety.  When  both 
varieties  are  combined  we  have  total  ophthalmoplegia,  in  which 
the  eyes  are  fixed  and  motionless,  the  pupils  being  immobile, 
both  varieties  of  reflex  nystagmus  (optic  and  vestibular)  being 
lost,  and  the  patient  can  look  in  any  particular  direction  only 
by  facing  his  head  that  way  en  bloc.  Nuclear  ophthalmoplegia, 
especially  external  ophthalmoplegia,  may  be  associated  with  motor 
paralysis  of  the  limbs  if  the  lesion  extends  ventrally  and  impli- 
cates one  or  other  pyramidal  tract,  or  it  may  be  associated  with 
involuntary  tremors  if  the  lesion  affects  the  red  nucleus  or  rubro- 
spinal tract  (Fig.  20,  p.  27). 

Sometimes  it  is  possible  to  differentiate  between  a  nuclear  and 
an  infra-nuclear  ocular  lesion.  In  the  case  of  paralysis  of  the  sixth 
nucleus  in  the  pons,  there  is  not  merely  weakness  of  the  external 
rectus  of  the  same  side,  as  in  paralysis  of  the  sixth  nerve  trunk, 
but  in  addition  the  internal  rectus  of  the  opposite  eye  is  paralysed, 
so  that  conjugate  movement  of  both  eyes  towards  the  affected 
side  is  impaired.  The  v  eakness  of  the  contra-lateral  internal 
rectus  is  only  in  connection  with  its  associated  movement  with 
the  external  rectus  of  the  ipso-lateral  eye.  This  is  proved  by 
the  fact  that,  in  paralysis  limited  to  the  sixth  nucleus,  both 
internal  recti  can  still  act  normally  dujing  convergence.  Again, 
since  the  facial  motor  root  loops  round  the  sixth  nucleus  within 
the  pons,  a  lesion  of  the  sixth  nucleus  is  not  infrequently 
accompanied  by  facial  paralysis  on  the  same  side.  The  sixth 
nucleus  is  essentially  an  oculogyre  centre,  turning  both  eyes  to 
the  corresponding   side,   and   therefore  controlhng   not  only  the 


150  NERVOUS    DISEASES 

external   rectus   of  the  ipso -lateral   side,   but    also   the    internal 
rectus  of  the  contra-lateral  side. 

With  regard  to  the  diagnosis  between  nuclear  and  infra-nuclear 
paralysis  of  the  third  nerve ;  if  in  a  doubtful  case  the  orbicularis 
oculi  is  found  to  be  afiected  together  with  the  external  ocular 
muscles,  then  the  lesion  is  in  the  region  of  the  nucleus,  since  the 
orbicularis  is  innervated  by  a  group  of  cells  which  are  in  anatomical 
proximity  to  the  oculomotor  nucleus  (but  which  really  belong  to 
the  facial). 

Mendel's  theory  ^  assumed  that  these  cells  belonged  to  the  oculo- 
motor nucleus  and  reached  the  orbicularis  through  the  facial,  but 
Bishop  Harman  ^  has  shown  that  all  the  facial  muscles,  from  orbi- 
cularis oculi  downwards,  are  innervated  from  the  group  of  cells  com- 
prising the  facial  nucleus,  the  upper  end  of  this  group  extending  as 
high  as  the  oculomotor,  and  the  lower  end  reaching  to  the  level  of  the 
hypoglossal. 

Sometimes  transient  ocular  palsy  affects  the  third  nerve  in 
whole  or  in  part,  recurring  in  the  same  eye  without  apparent 
cause  at  intervals  of  weeks  or  months,  and  clearing  up  com- 
pletely between  the  attacks.  This  condition,  known  as  migraine 
ophtalmo'plegique,  is  generally  associated  with  headache,  most 
intense  in  the  eye  and  forehead  of  the  affected  side,  and  with 
vomiting.  Its  pathology  is  obscure ;  probably  some  cases  are 
due  to  an  inflammatory  affection  of  the  meninges  at  the  point 
where  the  third  nerve  pierces  them  to  enter  the  sphenoidal  fissure. 
This  is  all  the  more  probable  inasmuch  as  the  first  division  of  the 
fifth  nerve,  which  traverses  the  sphenoidal  fissure,  is  often  simul- 
taneously affected,  with  the  result  that  there  is  blunting  of  sensa- 
tion in  its  area  of  distribution. 

Now  and  then  we  meet  with  congenital  ptosis,  in  which  there 
is  paralysis  of  the  superior  rectus  and  levator  palpebrse  superioris 
of  one  eye.  In  some  of  these  cases,  although  the  patient  cannot 
raise  his  upper  lid  voluntarily,  yet,  curiously  enough,  the  lid  is 
jerked  up  when  certain  jaw  movements  are  made,  particularly  when 
the  patient  throws  into  action  the  external  pterygoid  muscle  of  the 
same  side,  in  depressing  the  lower  jaw  towards  the  opposite  side. 

This  so-called  "jaw-winking"  movement  has  been  suggested  by 
Harman  to  be  the  survival  of  a  movement  in  fishes  whereby,  when 
the  mouth  is  opened  for  breathing  or  eating,  the  gill  swings  open. 

1  International  Med.  Congress,  Washington,  1887,  vol.  v.  p.  311. 
^  Transactions  of  Ophthalmological  Society,  1903,  p.  356. 


CRANIAL    NERVES 


151 


In  man  the  pterygoid  and  orbicularis  oculi  muscles  are  homologous 
with  the  deep  and  superficial  muscles  of  the  branchial  arch  of  the 
fish's  spiracle,  and  when  the  one  is  contracted  the  other  tends  to 
relax  and  "  the  weak  levator,  taking  advantage  of  the  quiescence 
of  its  too  powerful  opponent,  lifts  the  eyelid." 

Jaw-winking  movements  generally  disappear  before  adult  life. 

The  Fifth  or  Trigeminal  Nerve  has  an  extensive  distribu- 
tion, of  which  the  main  points  are  as  follows  : — 

The  nerve  consists  of  two  distinct  parts,  sensory  and  motor.  The 
sensory  root,  the  one  on  which  is  the  Gasserian  ganglion,  divides  below 


Great  OccipUxiL 

Nerve. 


FirslBiMisioTv 


SecondiDiyision/ 


SmaUbOccipUab 
Nerve 


AurvcularBranch, 

of  Vagus  o-rvci 

Ner  vus  interme-dujus 


Great  Avrijcular 
Nerve. 


.  ThirdBivisiorv 


CervicaLJferves 
Fig.  69.— Cutaneous  supply  of  head  (modified  from  Frolise). 

the  ganglion  into  three  divisions,  of  which  the  first  two  are  entirely 
sensory.  The  motor  root  courses  beneath  the  Gasserian  ganglion, 
and  then  joins  the  third  division,  which  thus  becomes  a  mixed  nerve. 

The  first  or  ophthalmic  division  passes  through  the  sphenoidal 
fissure  into  the  orbit  and  supplies  the  eyeball  and  lachrymal  gland, 
the  conjunctiva  (except  that  of  the  lower  lid),  the  skin  of  the  forehead 
and  scalp  up  to  the  vertex  (Fig.  69),  the  mesial  part  of  the  skin  of  the 
nose,  and  the  mucous  membrane  of  the  upper  part  of  the  nasal  cavity. 
It  also  contains  efferent  pupil-dilating  fibres  derived  from  the  cervical 
sympathetic,  joining  it  at  the  Gasserian  sanglion,  and  going  to  the 
iris  (Fig.  61). 

The  second  or  superior  maxillary  division  passes  through  the  foramen 
rotandum  across  the  spheno-maxillary  fossa  to  the  infra-orbital  canal. 
In  the  spheno-maxillary  fossa  it  is  connected  with  Meckel's  ganglion, 
which  gives  off  amongst  other  branches  the  Vidian  nerve.    This  latter 


152 


NERVOUS    DISEASES 


runs  backwards  to  join  the  facial  nerve,  the  posterior  end  of  the  Vidian 
being  named  the  great  superficial  petrosal  (Fig.  70).  The  superior 
maxillary  division  supplies  the  skin  of  the  upper  lip,  the  side  of  the 
nose  and  the  adjacent  part  of  the  cheek,  the  lower  eyelid  and  part  of 
the  temple.  It  also  supplies  the  conjunctiva  of  the  lower  lid,  the 
upper  teeth,  the  mucous  membrane  of  the  upper  lip,  the  upper  part 
of  the  cheek,  upper  jaw,  uvula,  tonsil,  naso-pharynx,  middle  ear  and 
lower  part  of  nasal  cavity.  It  also  contains  some  taste  fibres  to  which 
we  shall  refer  presently. 

The  third  or  inferior  maxillary  division  is  a  mixed  nerve.     It  emerges 
through  the  foramen  ovale.     The  motor  fibres  supply  the  masseter, 


Gassericcrv 
&ajigliorv 


Vnerye'  (sensory  root) 


Tongue, 


Genicuiaie  GangUoTv] 


Stylomastoid  fbrameti 
\t£riorAuricular 


GlossopharyngeaL 


Fig.  70. — Diagram  of  trigeminal,  facial,  and  glosso-pharyngeal  nerves, 
showing  course  of  taste  fibres. 

temporal,  and  both  pterygoid  muscles,  also  the  tensor  tympani,  mylo- 
hyoid and  anterior  belly  of  the  digastric.  The  sensory  fibres  supply 
the  skin  of  the  posterior  part  of  the  temple  and  adjacent  part  of  the 
pinna,  the  anterior  and  upper  wall  of  the  external  auditory  meatus, 
as  far  as  and  including  the  anterior  part  of  the  drum,  part  of  the  cheek, 
the  lower  lip  and  chin,  also  the  lower  teeth  and  gums,  the  tongue  (as 
far  back  as  the  circumvallate  papillae),  floor  of  mouth,  inner  surface 
of  cheek,  and  salivary  glands. 

The  Course  of  the  Taste  Fibres  is  a  complicated  one  and  still  much 
disputed  ^  (Fig.  70).  Those  for  the  anterior  two-thirds  of  the  tongue 
are  contained  in  the  lingual  nerve — a  branch  of  the  third  division.  But 
they  do  not  run  straight  up  from  the  lingual  into  the  fifth  nerve.     They 


1  Gushing,  Johns  Hopkins  Hospital  Bulletin,  1903,  Nos.  144-145.     Davies, 
Brain,  1907,  p.  219. 


CRANIAL    NERVES  153 

leave  the  lingual,  course  along  the  chorda  tympani,  and  reach  the  facial 
within  the  Fallopian  aqueduct.  They  run  in  the  facial  as  far  as  the 
geniculate  ganglion,  where  some  pass  off  along  the  great  superficial 
petrosal  to  Meckel's  ganglion,  ultimately  rejoining  the  fifth  nerve 
through  its  second  division.  Other  taste  fibres  leave  the  geniculate 
ganglion  to  enter  the  nervus  intermedins,  passing  thence  to  the  glosso- 
pharyngeal nucleus. 

The  taste  fibres  for  the  posterior  third  of  the  tongue  and  the  palate, 
which  are  supplied  by  the  glosso-pharyngeal  nerve,  probably  enter  the 
brain  through  the  glosso-pharyngeal.  They  do  not  join  tht  fifth  nerve, 
since  division  of  the  fifth  nerve  by  the  operation  of  removal  of  the 
Gasserian  ganglion  causes  impairment  of  taste  only  in  the  anterior 
two-thirds  of  the  tongue,  and  not  constantly  in  that.  Taste  is  not 
abolished  in  fifth  nerve  palsy,  as  was  formerly  thought,  for  in  several 
cases  of  my  own  I  have  found  that  the  patient,  though  unable  to  feel 
the  contact  of  food  or  other  objects  on  one  side,  still  retained  acute 
sense  of  taste  at  the  back  of  the  tongue. 

To  examine  the  sense  of  taste  we  direct  the  patient  to  protrude 
the  tongue,  and  we  lub  on  it  various  substances  such  as  sugar,  salt, 
quinine,  and  citric  acid,  preferably  in  wbite  powders,  which  the 
patient  cannot  distinguish  at  sight  one  from  the  other.  The  patient 
must  keep  his  tongue  protruded  throughout  each  test,  and  as 
soon  as  he  feels  a  taste  he  should  make  a  sign  and  also  determine 
in  his  mind  what  the  taste  is,  before  taking  the  tongue  in.  It  is 
convenient  to  have  a  card  with  the  following  words  printed  on 
it :— "  sweet,"  "  sour,"  "  bitter,"  "  salt,"  "  coppery."  The  patient 
can  then  point  with  his  finger  to  indicate  which  taste  he  per- 
ceives. If  he  be  allowed  to  pull  the  tongue  in  while  waiting  for 
the  sensation  to  arrive,  fallacies  may  occur  owing  to  movements 
of  the  tongue  and  the  flow  of  saliva  carrying  the  substance  to 
other  parts.  To  map  out  exactly  an  area  of  loss  of  taste  (ageusia) 
the  most  accurate  method  is  to  use  a  weak  galvanic  current  with  a 
wire  electrode,  which  produces  a  coppery  or  metalhc  taste. 

When  the  fifth  nerve  is  totally  paralysed  there  is  ansesthesia  of 
the  corresponding  half  of  the  face  and  scalp,  not  extending  as  far 
as  the  angle  of  the  jaw,  this  part  being  supphed  by  the  cervical 
plexus  (Fig.  69).  The  cornea  and  conjunctiva  on  the  affected 
side  are  anaesthetic,  and  also  the  mucous  membrane  of  the  corre- 
sponding side  of  the  nose,  mouth,  part  of  the  soft  palate  and  tongue, 
as  far  back  as  the  circumvallate  papillae  which,  with  the  area  behind, 
are  innervated  by  the  glosso-pharyngeal.  This  defect  extends 
exactly  to  the  middle  line,  and  therefore  the  patient  when  drink- 
ing feels  as  if  the  cup  were  broken.     Food  tends  to  collect  within 


154  NERVOUS    DISEASES 

the  anaesthetic  cheek,  the  buccinator  muscle  being  anaesthetic, 
though  its  motor  power  is  unaffected.  Taste  is  impaired  in 
the  anterior  two-thirds  of  the  tongue,  but  does  not  remain  totally 
lost.  The  trigeminal  nerve  has  also  sensory  fibres  for  the  facial 
muscles.  Hence  there  is  a  degree  of  awkwardness  and  apparent 
weakness  ol:  the  face — a  pseudo-facial  palsy,  due  to  loss  of  the 
sense  of  active  muscular  contraction.  AH  the  muscles  supplied 
by    the    motor    root    undergo     atrophic    paralysis    and    develop 


Fig.  71. — Paralysis  of  Left  third  and  of  Right  fifth  nerve.  The  patient  is 
looking  upwards  and  opening  the  jaw.  Showing  dilatation  of  pupil  on 
left  side  with  deficient  upward  movement  of  left  eye.  Also  showing 
the  deviation  of  the  lower  jaw  towards  the  right  side.  The  black  line 
indicates  area  of  anaesthesia  on  the  right  side  of  the  face. 

the  electrical  reactions  of  degeneration.  There  is  hollowing  of 
the  temporal  fossa  above  the  zygoma,  and  wasting  of  the 
masseter  below  it,  so  that  the  zygoma  becomes  abnormally 
prominent.  When  the  patient  clenches  his  teeth,  neither  the 
temporal  nor  the  masseter  can  be  felt  to  harden  as  on  the 
normal  side,  and  when  he  opens  his  mouth  the  mandible  is  pushed 
over  towards  the  paralysed  side  (Fig.  71).  This  is  owing  to  paralysis 
of  the  external  pterygoid,  which  fails  to  draw  the  condyle  forwards 
on  the  affected  side.  The  deflected  mandible  carries  with  it  the 
tongue,  but  there  is  no  real  deviation  of  the  tongue,  when  measured 
from  the  middle  line  of  the  lower  incisors.  Paralysis  of  the  mylo- 
hyoid is  sometimes  evidenced  by  a  relative  fiaccidity  upon  upward 


CRANIAL    NERVES 


155 


pressure  on  the  floor  of  the  mouth  on  the  affected  side.  It  is  stated 
that  paralysis  of  the  tensor  tympani  causes  a  difficulty  in  hearing 
notes  of  low  pitch,  but  this  is  not  easy  to  determine.  Secretion  of 
tears  on  the  paralysed  side  is  diminished,  as  is  also  the  secretion  of 
nasal  mucus  and  of  saliva.  Consequently  these  mucous  membranes 
become  abnormally  dry,  and  may  show  secondary  trophic  changes. 
Thus  stimulation  of  the  nasal  mucous  membrane  by  snuff  no  longer 
causes   sneezing.     Smell  at  first  is   unimpaired,   but  later,   from 


Fig.  72.  Fig.  72a. 

From  a  case  of  left-sided  facial  hemiatrophy.     Showing  atrophy  of 
corresponding  half  of  tongue. 

dryness  and  secondary  trophic  changes  in  the  Schneiderian  mem- 
brane, there  may  ba  anosmia  in  the  affected  nostril.  The 
corneal  and  lachrymal  reflexes  are  lost,  also  the  palatal  reflex,  and 
the  tongue  on  the  paralysed  side  becomes  excessively  furred,  pro- 
bably because  on  the  anaesthetic  side  there  is  deficient  friction  by 
food.  The  teeth  on  the  paralysed  side  are  anaesthetic  and  tend  to 
drop  out ;  this  has  been  ascribed  to  a  trophic  change,  but  more 
probably  it  is  mainly  traumatic,  the  patient  biting  clumsily  with 
his  anaesthetic  teeth.  It  used  to  be  stated  that  neuro-paralytic  kera- 
titis occurred  in  total  trigeminal  palsy,  owing  to  trophic  changes. 
But  this  is  not  invariably  so  ;    when  it  does  occur,  it  appears  to 


156  NERVOUS    DISEASES 

be  due  to  the  presence  of  a  special  bacillus  ^  in  the  anaesthetic 
eye,  where,  moreover,  there  is  a  deficiency  of  lachrymal  secretion. 
Further,  if  the  anaesthetic  Hds  be  kept  closed  by  a  suture,  keratitis 
does  not  occur,  even  though  the  special  bacillus  be  present. 

There  is  another  disease  which  occurs  in  the  territory  of  the 
fifth  nerve,  viz.,  progressive  facial  hemiatrophy.  This  disease,  which 
commences  in  early  life — usually  before  puberty,  and  more  often 
in  females  than  in  males — shows  itself  first  in  the  skin  of  the 
face,  either  near  the  orbit  or  over  the  upper  or  lower  jaw,  gradually 
spreading  over  the  whole  face  on  one  side.  The  skin  becomes 
thinned  from  atrophy  of  its  papillary  layer,  the  subcutaneous  fat 
disappears,  and  thus  the  affected  side  of  the  face  becomes  wrinkled 
and  furrowed,  in  marked  contrast  with  the  healthy  side.  Later 
the  subjacent  muscles,  cartilages,  and  bones  become  atrophic,  but 
without  motor  paralysis  or  reaction  of  degeneration.  The  corre- 
sponding side  of  the  tongue  (Figs.  72a  and  159a),  and  occasionally 
that  of  the  soft  palate,  also  become  wasted.  But  the  hemi-atrophied 
tongue,  when  protruded,  comes  out  straight,  unhke  that  of  a  patient 
with  atrophy  from  hypoglossal  palsy  (Fig.  84,  p.  178).  The  hair  on 
the  affected  side  of  the  face  may  fall  out  or  become  white,  and  the 
sebaceous  glands  may  atrophy.  The  scalp  is  rarely  affected.  There 
is  no  anaesthesia. 

The  area  of  this  disease  corresponds  accurately  with  that  of  the 
distribution  of  the  fifth  nerve,  and  in  certain  cases  pathological  changes 
have  been  found  either  in  the  nerve  itself  or,  more  constantly,  in  its 
nucleus  of  origin.  Thus  Mendel  found  signs  of  neuritis  in  the  nerve, 
together  with  changes  in  the  spinal  root  of  the  fifth  within  the  medulla. 
More  recently  Loebl  and  Wiesel  ^  found  an  interstitial  neuritis  of  the 
Gasserian  ganglion  and  of  the  parts  distal  to  it.  Removal  of  the 
Grasserian  ganglion  does  not  produce  hemiatrophy. 

Facial  hemiatrophy  may  also  be   a  symptom  of  syringobulbia, 

1  Davies  and  Hall,  British  Medical  Journal,  1908,  p.  72. 

^  Deutsche  Zeitschrift  filr  Nervenheilkunde,  1904,  Bd.  27,  s.  355. 


CHAPTER   X 

CKANIAL  NERVES  {continued) 

Of  all  tlie  peripheral  nerves  in  the  body,  cranial  or  spinal,  the 
Seventh  or  Facial  nerve  is  by  far  the  most  frequently  paralysed, 
hence  the  importance  of  knowing  its  anatomical  course  and  dis- 
tribution. Like  the  trigeminal,  it  is  a  mixed  nerve,  possessing  a 
motor  root — the  facial  nerve  proper,  and  a  sensory  root — the 
nervus  intermedius  of  Wrisberg.  These  two  roots  meet  at  the 
geniculate  ganglion. 

Let  us  first  consider  the  motor  root.  Arising  from  a  nucleus 
situated  mainly  in  the  lower  part  of  the  pons,  but  some  of  whose 
cells  (namely,  those  for  the  orbicularis  oculi)  extend  as  high  as  the  nucleus 
of  the  third  nerve,  and  others  (namely,  those  for  the  orbicularis  oris) 
are  as  low  as  the  hypoglossal  nucleus,  the  motor  root  of  the  facial 
pursues  a  tortuous  course.  Firstly,  within  the  substance  of  the  pons 
it  forms  a  loop  which  hooks  round  the  nucleus  of  the  sixth  nerve. 
Then,  leaving  the  ventral  surface  of  the  brain-stem,  it  enters  the  in- 
ternal auditory  meatus,  and  passes  along  a  winding  bony  canal  in  the 
temporal  bone — the  aqueduct  of  Fallopius.  In  the  upper  part  of  this 
canal  it  traverses  a  swelling,  the  geniculate  ganglion,  which  is  joined 
by  the  sensory  root  or  portio  intermedia  of  Wrisberg,  also  by  the  great 
superficial  petrosal  nerve  from  Meckel's  ganglion,  and  by  the  small 
superficial  petrosal  from  the  otic  ganglion  (see  Fig.  70).  The  geniculate 
ganglion  is  similar  in  structure  to  a  posterior  root  ganglion  and  is 
sensory  in  function.  Inflammation  of  this  ganglion  is  accompanied 
by  herpes  of  the  external  auditory  canal  and  adjacent  part  of  the 
auricle,  exactly  analogous  to  herpes  zoster  ^  (see  Fig.  69,  p.  151). 
Within  the  aqueduct  the  facial  gives  off  a  branch  to  the  stapedius, 
and,  lower  down,  the  chorda  tympani  leaves  it  to  join  the  lingual 
nerve.  It  then  emerges  from  the  skull  through  the  stylo-mastoid 
foramen,  giving  off  a  posterior  auricular  branch  to  the  muscles  of  the 
pinna  and  to  the  occipital  belly  of  the  occipito-frontalis.  The  main 
trunk  then  divides  into  its  terminal  branches  supplying  all  the  muscles 
of  the  face  (except  the  levator  palpebree  superioris)  from  the  frontalis 
above  to  the  platysma  below.  It  also  supplies  the  stylo-hyoid  and 
posterior  belly  of  the  digastric. 

^  J.  Ramsay  Hunt,  Journal  of  Nervous  and  Mental  Diseases,  1907,  p.  73. 

157 


158 


NERVOUS    DISEASES 


Although  the  facial  nerve  is  largely  motor,  the  geniculate  ganglion 
is  a  sensory  ganglion.  The  facial  also  contains  "  autonomic  "  secre- 
tory fibres,  whilst  the  taste-fibres  of  the  chorda  tympani  accompany 
the  motor  portion  of  the  nerve  in  part  of  its  course.  Thus  lesions 
at  different  levels  can  be  distinguished  one  from  the  other. 

1.  If  the  facial  nerve  is  affected  after  its  exit  from  the  stylo-mastoid 
foramen,  e.g.  by  cold,  or  by  injuries  or  tumours  in  that  region,  the 
result  (Bell's  Paralysis)  is  complete  palsy  of  that  side  of  the  face, 


Case  of  left-sided  facial  palsy.     Fig.  73  at  rest.     Fig.  73a  on  attempt  to 
close  eyes  and  retract  angles  of  mouth. 

which  is  therefore  asymmetrical  at  rest,  and  the  asymmetry  is 
exaggerated  on  voluntary  movement.  The  patient  has  neither 
emotional  nor  voluntary  movement  of  the  affected  side  (Figs.  73 
and  73a). 

The  furrows  of  the  forehead  are  wiped  out,  and  the  patient 
cannot  wrinkle  the  brow  nor  frown  on  that  side.  The  eye  is  more 
widely  open  on  the  affected  side  and  cannot  be  shut.  The  tears 
run  down  the  cheek  instead  of  into  the  lachrymal  duct,  and  may 
produce  excoriation  of  the  skin  or  eczema.  When  the  patient 
tries  to  shut  the  eye  he  merely  rolls  the  eyeball  upwards  and 
outwards,  or  upwards  and  inwards,  sometimes  with  a  zig-zag 
movement,  until  the  cornea  passes  under  cover  of  the  upper  lid. 
An  additional  sign,  the  "  levator  "  sign,  pointed  out  by  Dutemps 


CRANIAL    NERVES  159 

and  Cestan,^  is  as  follows  :— When  the  patient  looks  down  and 
then  attempts  to  shut  both  eyes  slowly,  the  upper  lid  on  the 
paralysed  side  is  seen  to  move  up  a  little  (see  Figs.  74  and  74a), 
owing  to  contraction  of  the  levator  palpebrae,  which  normally  acts 
synergically  with  the  orbicularis  but  is  now  no  longer  antagonised 
by  it.  Another  sign  is  Negro's  ^  hyper-kinetic  sign  of  the  eyeball 
and  upper  lid.  When  the  patient  looks  upwards  to  the  full  extent, 
the  two  eyeballs  become  asymmetrically  placed.     On  the  paralysed 


Fig.  74.  .  Fig.  74a. 

Fig.  74. — Case  of  right-sided  facial  palsy  :  patient  looking  downwards 

at  observer's  finger. 

Fig.  74A. — The  patient  closes  both  eyes:  observe  the  elevation  of 

the  right  upper  lid. 

side  the  globe  deviates  outwards  and  then  comes  to  rest  at  a  higher 
level  than  on  the  normal  side,  probably  owing  to  over-innervation 
of  the  superior  rectus  muscle. 

The  inability  to  close  the  eye  allows  the  entrance  of  foreign 
bodies,  and  consequently  conduces  to  conjunctivitis.  The 
corneal  reflex  is  abolished,  and  the  regular  involuntary  blinking 
of  health  no  longer  occurs  on  the  paralysed  side.  The  eye  brims 
over  with  tears,  so  that  vision  on  the  affected  side  is  rendered  less 
acute.  Curiously  enough,  though  the  eye  caimot  be  shut  during 
waking  hours,  during  sleep  it  often  closes  almost  completely, 
probably  from  relaxation  of  the  levator  palpebrse. 

1  Journal  de  Neurologic,  1904,  p.  48. 

-  de  Castro,  Revue  neurologique,  19.3,  No.  3,  p.  149. 


160  NERVOUS    DISEASES 

The  tip  of  the  nose  is  drawn  somewhat  towards  the  sound  side, 
the  naso -labial  fold  on  the  affected  side  is  flattened  out,  the  ala  nasi 
sinks  in  and  shows  no  active  movement,  voluntary  or  respiratory, 
though  it  may  flap  passively  during  forcible  nasal  breathing.  The 
mouth  is  drawn  towards  the  sound  side,  but  on  the  affected  side  its 
angle  droops  and  saliva  dribbles  from  it.  When  the  patient  smiles 
or  shows  the  upper  teeth,  the  healthy  side  moves  alone  ;  he  cannot 
whistle,  and  the  articulation  of  labial  consonants  is  impaired. 
During  mastication  food  accumulates  between  the  teeth  and  the 
paralysed  cheek.  The  patient  often  bites  his  cheek  or  lower  lip,  and 
during  forcible  blowing  expiration  the  paralysed  cheek  flaps  loosely. 
Voluntary  movement  of  the  integument  by  the  platysma,  as  in 
forcible  depression  of  the  chin  against  resistance,  is  abolished  on.  the 
affected  side.  In  those  patients  who  were  previously  able  to  move 
the  ear  voluntarily,  that  power  is  also  lost.  All  the  paralysed  muscles 
gradually  develop  the  electrical  reactions  of  degeneration.  The 
affected  side  of  the  face  generally  sweats  less  than  the  healthy 
side. 

2.  If  the  lesion  be  within  the  Fallopian  aqueduct  below  the 
geniculate  ganglion,  it  produces  all  the  above  symptoms,  and,  in 
addition,  from  implication  of  the  chorda  tympani,  there  is  loss 
of  taste  (and  sometimes  slightly  of  common  sensation)  in  the 
anterior  two-thirds  of  the  tongue  on  the  affected  side,  and  also 
occasionally  abnormal  subjective  sensations  of  taste,  and  sometimes 
diminution  or  excess  of  submaxillary  and  sublingual  sahva.  The 
deficiency  of  taste  and  of  saliva  may  cause  this  part  of  the  tongue  to 
be  abnormally  furred  up  to  the  middle  line.  If  there  be  paralysis 
of  the  nerve  to  the  stapedius,  there  is  hyperacousis  or  painful 
sensitiveness  to  loud  sounds  ^  (presuming  that  the  auditory 
apparatus  is  not  affected),  and  the  patient  can  no  longer 
produce  the  subjective  noise  in  the  ear,  which  we  normally  hear 
on  attempting  very  forcibly  to  innervate  the  facial  muscles,  espe- 
cially the  orbicularis  palpebrarum. 

3.  If  the  motor  root  of  the  nerve  be  affected  between  its 
emergence  from  the  pons  and  the  geniculate  ganglion,  it  produces 
the  same  symptoms  as  in  Bell's  paralysis,  but  without  affection  of 
taste  in  the  front  of  the  tongue.  And  since  disease  in  this  region 
almost  invariably  implicates  the  auditory  nerve,  there  is  usually 

1  Moos  {Zeitschrift  fur  Ohrenheilk uncle,  vol.  viii.  p.  221)  records  a  case  in  wLich 
the  hyperacousis  was  specially  for  low-pitched  notes. 


CRANIAL    NERVES 


161 


deafness  also.     If  the  auditory  nerve  chances  to  escape,  hyperacousis 
will  occur  from  stapedius  paralysis.     Many  cases  have  deficiency 


A> 


// 


/  // 


Tears  ^ 
Taste&SaJbira.l 


Grec^Stiper^ciall  Joenlcalateaanfflwn. 


•Tears 

'  Taster  SiSaJiva/ 


PostJluricular 

Nerx'e/ 


Fig.  75. — Diagram  of  Facial  Nerve,  showing  course  of  secretory  and  of 
taste-fibres. 


162  NERVOUS    DISEASES 

of  tears  on  the  afiected  side.  Most  cases  of  basal  intra-cranial 
disease  present  general  symptoms  also,  such  as  headache,  giddiness 
and  vomiting. 

4.  If  the  lesion  of  the  motor  root  be  within  the  substance 
of  the  pons,  facial  palsy  results  as  in  Bell's  paralysis,  but 
taste  and  hearing  are  unaffected.  There  is,  however,  usually 
an  accompanying  paralysis  of  the  sixth  nerve  or  its  nucleus, 
since  the  facial  motor  root  hooks  round  the  sixth  nucleus  within 
the  pons. 

Paralysis  of  the  soft  palate  used  to  be  included  in  the  symptoms  of  a 
lesion  of  the  facial  nerve  at  or  above  the  geniculate  ganglion.  But  the 
■weight  of  evidence  goes  to  prove  that  the  facial  has  no  share  in  the  innerva- 
tion of  the  palate.  Chvostek,^  in  1883,  published  a  case  of  sarcoma  of  the 
facial  nerve  in  which  paralysis  of  the  palate  had  been  observed,  but  that 
was  before  the  days  of  the  Marchi  method,  and  it  is  impossible  to  be  sure 
that  the  lower  roots  of  the  vagus  Avere  undegenerated.  In  his  case  there  was 
also  a  cancer  in  the  tongue. 

Slight  cases  of  facial  palsy,  whether  due  to  cold,  middle-ear 
affection,  compression,  or  other  causes,  may  recover  completely 
in  one  or  two  weeks.  More  severe  cases  last  from  two  to  eight 
months  before  recovery  begins.  Or  the  palsy  may  remain  perma- 
nent. In  severe  cases,  in  which  improvement  does  not  begin  for 
three  months  or  more,  a  spastic  or  contractured  condition  usually 
comes  on  as  voluntary  power  reappears.  The  mouth  becomes 
drawn  back  again  towards  the  paralysed  side,  the  palpebral  fissure 
instead  of  being  wider,  is  narrower  than  on  the  healthy  side,  and 
the  naso-labial  and  other  furrows  not  only  reappear,  but  become 
exaggerated.  The  result  is  that,  when  at  rest,  the  healthy  side  may 
seem  the  weaker  of  the  two,  though  when  voluntary  movement 
takes  place  it  is  easy  to  see  which  is  the  affected  side  (see  Figs. 
76  and  76a).  Together  with  this  contracture  there  is  always 
in  the  spastic  muscles  a  tendency  to  over-action,  imperfect 
recovery  being  associated  with  imperfect  control.  One  variety  of 
facial  hemi-spasm  results  (see  p.  103).  Thus,  on  closing  the  eye 
on  the  affected  side,  the  angle  of  the  mouth  becomes  drawn  out- 
wards ;  or  again,  on  showing  the  upper  teeth,  the  eye  becomes 
closed.  Sudden  flickers  of  involuntary  fibrillary  tremors  may 
sometimes  be  seen  on  the  affected  side.  The  spastic  facial  muscles 
can  also  be  made  to  contract  reflexly  by  tapping  lightly  over  the 

'  Wiener  medizinische  Presse,  1883,  s,  34. 


CRANIAL    NERVES 


163 


point  of  emergence  of  the  most  accessible  branch  of  the  fifth,  viz., 
the  supraorbital  nerve/ 

Secondary  contracture  occurs  only  in  cases  of  incomplete  re- 
covery. During  the  stage  of  total  paralysis,  when  no  impulses  are 
reaching  them,  the  muscles  are  quite  flaccid.  The  development  of 
contracture  indicates  that  muscular  regeneration  has  been  imperfect. 

Bilateral  facial  falsy  is  rare.  It  may  be  due  either  to  intra- 
or  extra-cranial  causes,  the  commonest  intra-cranial  cause  being 


Case  of  left-sided  facial  palsy  with  contracture.     Fig.  7G  shows  position  at  rest. 
Fig.  7<)A  shows  maximum  voluntary  movement. 

gummatous  basal  meningitis.  Of  the  extra-cranial  causes,  the 
most  important  are  double  otitis  media,  cold,  and  post-diphtheritic 
paralysis.  Alcohohc  paralysis  rarely  attacks  the  facial  nerve,  but 
when  it  does,  the  affection  is  bilateral,  as  in  the  case  of  the 
man  shown  in  Figs.  77  and  77a,  who  also  had  typical  alcoholic 
neuritis  of  the  limbs. 

In  bilateral  facial  palsy  there  is  no  asymmetry  of  the  face,  but 
it  hangs  like  a  fixed  expressionless  mask,  incapable  of  evincing 
the  shghtest  emotion. 

Bilateral    facial  weakness  also   occurs  in  the   "  facio-scapulo- 


Mondino,  Rivista  di  pafologia  nervosa  e  mentale,  1907,  p.  49. 


164 


NERVOUS    DISEASES 


humeral "  type  of  myopathy,  to  which  we  shall  refer  in  a  later 
chapter. 

Nervus  Intermedius  of  Wrisberg,  or  Sensory  Root  of  the 
Facial. — Between  the  facial  motor  root  and  the  auditory  nerve  at 
the  floor  of  the  cranial  cavity,  and  entering  the  internal  auditory 
meatus  along  with  them,  there  is  a  slender  fasciculus,  known  as  the 
fortio  intermedia. 

The  fibres  of  this  nerve  are  remarkably  small  in  calibre.  Their  trophic 
centre  is  in  the  cells  of  the  geniculate  ganglion.  Centrally  the  fibres  run 
into  the  bulb,  alongside  the  fibres  of  the  auditory  nerve,  to  join  a  nucleus 


Fig. 


Fig.  77A. 


Fig.  77. — Bilateral  facial  palsy,  alcoholic  in  origiu,  associated  with  peripheral 

neuritis  of  upper  and  lower  limbs. 
Fig.  77a. — Maximum  voluntary  movement  of  face,  on  attempt  to  close  the 

eyes  and  to  retract  angles  of  mouth. 


closely  connected  with  that  of  the  glosso-pharyngeal.  Peripherally  from 
the  geniculate  ganglion  fibres  run  along  the  great  and  small  superficial 
petrosal  nerves  ;  others  along  the  trunk  of  the  facial,  in  the  chorda 
tympani. 

The  nervus  intermedius  probably  conveys  taste  impulses  up- 
wards to  the  brain,  by  way  of  the  glosso-pharyngeal  nucleus 
(Fig.  75,  p.  161).  It  also  contains  autonomic  efferent  fibres 
which  join  the  submaxillary  ganglion.  Inflammation  of  the 
geniculate  ganglion,   analogous   to  inflammation  of  the    posterior 


CRANIAL    NERVES  165 

root  ganglion  in  herpes  zoster,  as  Hunt  has  pointed  out,  pro- 
duces characteristic  symptoms.  These  consist  in  pain  and  herpes 
of  the  auricle  and  external  auditory  canal.  If  the  inflammation 
be  intense  enough  to  implicate  the  motor  fibres  of  the  facial  there 
is  facial  palsy  also,  with  loss  of  taste  in  the  chorda  tympani 
distribution.  If  the  auditory  nerve  be  implicated  there  is 
vertigo,   tinnitus,  deafness  and  even  nausea  and  vomiting.^ 

The  Eighth  or  Auditory  Nerve  comprises  two  entirely 
different  sets  of  fibres.  (See  Fig.  30,  p.  48.)  Firstly,  there  are 
cocJdear  fibres  from  the  auditory  labyrinth,  subserving  the  function 
of  hearing.  Secondly,  there  are  vesiibuhr  fibres  from  the  semi- 
circular canals  or  static  labyrinth.  These  constitute  the  most 
important  nerve  of  equiUbration,  informing  us  of  the  position 
of  our  head  in  space.  Affections  of  the  cochlear  fibres  produce 
auditory  phenomena,,  while  disease  of  the  vestibular  fibres  causes 
one  form  of  vertigo,  though  vertigo  and  other  auditory  symptoms 
often  result  not  only  from  disease  of  the  labyrinth  or  vestibular 
fibres,  but  from  affections  of  the  middle  or  even  of  the  outer  ear. 
The  chief  symptoms  referable  to  the  auditory  nerve  are  deaf- 
ness, tinnitus  and  vertigo. 

In  a  patient  who  is  apparently  deaf  we  should  always,  before 
proceeding  to  test  the  hearing,  examine  the  external  auditory 
meatus,  to  make  sure  that  it  is  not  blocked,  e.g.  by  wax.  We 
then  test  aerial  conduction  by  the  ticking  of  a  watch,  the 
patient's  eyes  being  shut  and  one  ear  closed  while  the  other 
is  being  tested.  Holding  the  watch  at  some  distance  from 
the  ear,  we  slowly  bring  it  nearer  until  the  patient  can  just  detect 
the  tick.  If  there  is  deafness,  we  have  to  determine  whether 
this  is  due  to  middle- ear  disease  or  to  affection  of  the  labyrinth 
or  auditory  nerve.  The  tuning- fork  tests  help  us  here.  Normally 
a  vibrating  tuning-fork,  preferably  C^  ( =  256  vibrations  per  second), 
placed  on  the  vertex  or  centre  of  the  forehead,  is  heard  equally  in 
both  ears  (Weber's  test),  and  if  one  ear  be  temporarily  closed  by 
the  finger,  the  note  is  heard  louder  on  that  side.  If  the  tuning- 
fork  be  placed  on  the  mastoid  process,  we  wait  till  it  is 
no  longer  heard  through  the  bone,  and  find  normally  that  it 
is  still  audible  when  held  close  to  the  external  meatus  (Rinne's 
test).  If  the  middle  ear  be  diseased,  or  if  the  outer  ear  be  blocked 
up,  there  is  loss  of  aerial  conduction,  but  bone-conduction  is  still 

1  See  a  case  by  Arthur  Cheatle,  Trans.  Otological  Soc,  vol.  ii.  p.  6. 


166  NERVOUS    DISEASES 

preserved.  The  tuning-fork  on  the  vertex  is  then  heard  louder  on 
the  affected  side  ("  positive-Weber,")  and  Rinne's  test  is  negative, 
i.e.  the  tuning-fork  is  no  longer  heard  aerially  after  fading  away  on 
bone-conduction.  But  if  the  deafness  be  due  to  affection  of  the 
internal  ear  or  of  the  auditory  nerve — so-called  "  nerve-deafness," 
a  tuning-fork  on  the  vertex  is  not  heard  on  the  affected  side 
("  negative -Weber  "),  whilst  as  a  rule  there  is  "  positive -Rinne," 
though  not  always.  In  deafness  from  chronic  middle-ear  catarrh, 
the  hearing  is  generally  better  in  the  midst  of  a  noise  {e.g.  in  an 
omnibus  or  railway  carriage),  than  in  a  quiet  place  : — so  called  ^ar- 
acousis  Willisii,^  whereas  in  nerve -deafness  the  reverse  is  the  case. 
Additional  localising  evidence  may  also  be  obtained  from  the  other 
concomitant  symptoms.  Thus  gross  disease  of  the  auditory  nerve 
within  the  skull,  e.g.  in  a  case  of  lateral  extra-cerebellar  tumour, 
is  often  accompanied  by  facial  paralysis,  though  this  conjunction 
is  of  value  only  when  middle-ear  disease  can  be  excluded.  On  the 
other  hand,  disease  of  the  labyrinth  is  often  associated  with  tinnitus 
or  vertigo,  and  labyrinthine  deafness  is  specially  characterised  by 
loss  of  perception  for  high-pitched  tones,  as  tested  by  Galton's 
whistle.  Disease  of  the  auditory  nuclei  within  the  pons  may  be 
associated  with  weakness  of  the  motor  facial  nerve  of  the  same 
side  and  paralysis  of  the  opposite  arm  and  leg. 

Tinnitus,  or  ringing  in  the  ears,  is  a  subjective  symptom.  It 
signifies  irritation  of  some  part  of  the  auditory  apparatus.  The 
term  does  not  include  elaborate  auditory  hallucinations  of  cortical 
origin,  such  as  distinct  melodies  or  voices  uttering  intelligible 
words.  The  nature  of  the  sound  in  tinnitus  varies  in  different 
cases ;  for  example,  it  may  be  buzzing,  hissing  or  whistling. 
Broadly  speaking,  we  recognise  two  main  kinds  of  tinnitus — the 
pulsating  and  the  continuous.  Pulsating  sounds,  synchronous  with 
the  pulse,  occur  in  a  few  intra-cranial  aneurisms  (sometimes 
audible  by  the  physician  on  auscultation  of  the  skull),  but  are  also 
not  infrequent  in  simple  neurasthenia  in  the  "  silent  watches  of  the 
night,"  and  in  temporary  Eustachian  obstruction,  as  in  some  cases 
of  coryza.     Curious  "  clicking  "  sounds  in  the  ear  may  result  from 

1  Paracousis,  according  to  some  observers,  is  associated  with  abnormally  low 
labyrinthine  pressure,  and  the  temporary  improvement  of  hearing  in  such 
patients  during  a  noisy  journey,  in  a  railway  carriage  or  motor  car,  is  due  to  a 
reflex  contraction  of  the  stapedius  muscle  pushing  inwards  the  foot  of  the  stapes 
and  raisins:,  for  the  time  being,  the  pressure  of  the  endolymph  (see  A.  Cheatle, 
Trans.  Otol.  Soc,  1900,  vol.  i.  p.  52  ;  also  C.  Heath). 


CRANIAL   NERVES  167 

clonic  spasm  of  the  tensor  tympani  muscle.  Continuous  sounds 
may  be  of  high  or  low  pitch.  We  should  always  notice  whether 
they  are  increased  or  diminished  by  the  recumbent  posture.  Low- 
pitched  continuous  tinnitus  may  be  the  result  of  venous 
hypersemia,  in  which  case  it  is  aggravated  by  recumbency,  or 
of  simple  anaemia,  which  is  relieved  by  lying  down.  Nitrite 
of  amyl  aggravates  tinnitus  when  due  to  hyperemia  and  relieves 
it  when  due  to  anaemia.  High-pitched  continuous  tinnitus  is 
generally  due  to  labyrinthine  stimulation,  either  from  outer  or 
middle-ear  affection  (perhaps  merely  wax  or  water  in  the  external 
meatus,  an  obstructed  Eustachian  tube,  or  an  indrawn  tympanic 
membrane),  or  from  actual  labyrinthine  disease.  It  is  also  caused 
by  certain  drugs,  notably  by  quinine  and  salicylates.  Such  drugs 
induce  deafness  as  well  as  tinnitus,  and  the  tinnitus  may  persist 
for  weeks  after  the  deafness  has  cleared  up.  Pulsating  tinnitus 
due  to  arterial  congestion  can  often  be  arrested  temporarily  by 
compression  of  the  vertebral  artery  supplying  the  labyrinth,  or  of 
the  carotid  supplying  the  external  or  middle  ear.^ 

Vertigo,  or  giddiness,  is  the  peculiar,  disagreeable  sensation 
which  results  if  our  sense  of  secure  equilibration  is  disturbed.  The 
process  of  equilibration  is  a  muscular  act,  in  which  all  the  muscles 
in  question  are  innervated,  of  course,  by  the  cerebral  cortex,  this 
latter  being  again  largely  influenced  by  the  cerebellum.  The 
cerebellum  is  a  co-ordinating  centre  for  equihbration.  It  receives 
afferent  impulses  from  various  sources,  of  which  the  semicircular 
canals  of  the  inner  ear  are  by  far  the  most  important,  the  others 
coming  from  the  skin  of  those  parts  on  which  the  body  happens  to 
be  resting,  from  the  muscles  and  joints  concerned  in  maintaining 
our  balance,  and  from  the  muscles  of  the  head  and  eyes  con- 
cerned in  looking  ''towards  surrounding  objects.  Each  half  of 
the  cerebellum  exercises  a  co-ordinating  influence,  through  the 
corresponding  superior  cerebellar  peduncle,  upon  the  contra-lateral 
cerebral  cortex,  and  thus  upon  the  muscles  of  the  ipso-lateral  Hmbs. 

Giddiness  is  often  accompanied  by  a  feeling  of  movement 
either  in  the  patient  himself  (subjective  vertigo)  or  in  external 
objects  (objective  vertigo).  Severe  giddiness  usually  produces  the 
motor  phenomenon  of  reeling  or  staggering. 

Vertigo  may  result  from  affection  either  of  the  higher  cerebral 
centres  or  of  the  co-ordinating  cerebellar  centres,  or  from  affection 

1  Dundas  Grant,  Brit.  Med.  Journal,  Dec.  24,  1887. 


168  NERVOUS    DISEASES 

of  any  of  the  afferent  paths  to  which  we  have  already  referred. 
Severe  vertigo  is  often  accompanied  by  nausea  and  vomiting,  as  in 
sea-sickness. 

Vertigo  may  occur  in  healthy  people.  Thus,  for  example,  a 
galvanic  current  of  10  to  15  milliamperes  passed  transversely 
through  the  head  produces  a  variety  of  giddiness  probably  due  to 
labyrinthine  stimulation.  In  this  galvanic  vertigo  the  patient 
tends  to  walk  or  fall  towards  the  side  of  the  positive  pole,  and  his 
head  and  eyes  are  also  rotated  in  that  direction,  accompanied  by 
a  rotatory  nystagmus,  until  the  moment  of  stopping  the  current, 
when  he  tends  to  fall  towards  the  side  of  the  negative  pole.  Rapid 
rotation  of  the  body  round  its  own  axis,  as  in  waltzing,  or  rapid 
changes  in  our  position  in  space,  as  in  swinging,  produce  giddiness 
which  is  probably  due  to  variations  in  the  pressure  of  the  endolymph 
within  the  semicircular  canals.  Some  people  feel  giddy  when 
stepping  unexpectedly  from  a  firm  surface  on  to  a  piece  of  boggy 
turf,  or,  as  in  a  famous  Edinburgh  street,  on  to  a  piece  of  india- 
rubber  pavement,  this  variety  of  vertigo  being  due  to  deficient 
sense  of  resistance  conveyed  from  the  skin  of  the  soles  and  from 
the  muscles  and  joints  of  the  lower  limbs.  The  giddiness  produced 
by  standing  near  the  edge  of  a  cliff  or  of  a  high  tower  is  most 
probably  due  to  loss  of  muscular  impression  from  the  ocular 
muscles.  Ordinarily  we  have  surrounding  objects  at  or  above  our 
own  level  with  which  to  compare  our  position  in  space,  and  if 
such  objects  are  absent,  vertigo  may  result. 

Vertigo  is  also  associated  with  various  pathological  conditions. 
Among  the  intra -cranial  causes  we  may  mention  blows  on  the 
head  (this  variety  is  often  relieved  by  repeated  small  doses,  about 
ttV  grain,  of  perchloride  of  mercury),^  and  sudden  cerebral  anoemia  or 
hypercemia.  A  distinguished  member  of  the  medical  profession 
who  was  the  subject  of  aortic  regurgitation  used  to  have  attacks  of 
intense  vertigo  if  he  took  a  saline  aperient.  Probably  in  his  case 
the  withdrawal  of  a  considerable  amount  of  fluid  from  the  circula- 
tion rendered  the  brain  anaemic — hence  the  vertigo.  It  was  always 
relieved  by  the  recumbent  posture,  while  cardiac  tonics  and  the 
avoidance  of  hydragogue  cathartics  prevented  its  recurrence. 
Vertigo  from  cerebral  hypergemia  is  very  common  in  women  about 
the  menopause,  also  in  the  arterio -sclerosis  of  chronic  renal  disease. 
In  the  latter  class,  relief  is  often  obtained  by  the  administration  of 

1  Dunclas  Grant,  Clinical  Journal,  Oct.  9,  1907.  , 


CRANIAL    NERVES  169 

iodides.  It  is  still  more  marked  in  many  cases  of  cerebral  hasmor- 
rhage  or  thrombosis,  of  which  it  may  be  a  premonitory  signal. 
Griddiness  in  old  people  with  atheromatous  arteries,  if  it  be 
associated  with  headache,  and  especially  if  there  be  no  sign 
of  labyrinthine  disease,  should  always  be  regarded  seriously. 
Intra-cranial  tumours  may  cause  giddiness  by  raising  the  general 
pressure  within  the  skull,  and  cerebellar  tumours  are  especially 
associated  with  vertigo,  even  apart  from  increased  intra-cranial 
pressure.  Intra- cerebellar  tumours  of  the  lateral  lobe  produce  a 
vertigo  in  which  the  subjective  sense  of  rotation  of  the  body  is  in 
the  same  direction  as  that  of  the  apparent  movement  of  surrounding 
objects,  i.e.  away  from  the  side  of  the  lesion.  In  extra-cerebellar 
tumours,  while  external  objects  appear  to  move  away  from  the 
side  of  the  lesion,  the  sense  of  subjective  rotation  is  reversed,  i.e. 
towards  the  side  of  the  lesion. 

A  characteristic  form  of  vertigo  has  also  been  described  by 
Bruns,^  and  confirmed  by  various  other  observers.^  It  is  pro- 
duced by  the  presence  of  a  cysticercus  in  the  fourth  ventricle. 
Sometimes  the  worm  is  anchored  to  the  ependyma,  sometimes  it 
is  swimming  free.  The  patient,  who  otherwise  shows  no  sign  of 
intra-cranial  organic  disease,  has  paroxysms  of  violent  vertigo, 
chiefly  on  sudden  movement  of  the  head,  either  active  or  pas- 
sive, causing  a  temporary  shifting  of  the  position  of  the  worm. 
He  also  has  attacks  of  occipito -frontal  headache  with  vomiting ; 
his  gait  is  tottering  and  unsteady,  and  glycosuria  is  not  uncom- 
monly present.  The  cerebro- spinal  fluid  may  show  eosinophilia,  a 
sign  which  is  practically  pathognomonic,  and  there  is  usually 
also  an  increase  of  eosinophiles  in  the  circulating  blood.  There 
may  be  intervals  during  which  he  is  apparently  well,  and  the  case 
may  be  mistaken  for  hysteria.  Death  usually  occurs  suddenly 
from  respiratory  paralysis. 

Vertigo  is  associated  with  certain,  degenerative  diseases,  notably 
with  disseminated  sclerosis.  Vertigo  is  frequently  the  "aura" 
of  an  epileptic  fit,  or  may  accompany  the  headache  of  an  attack 
of  migraine.  A  hereditary  family  form  of  giddiness  has  also 
been  described. 

Toxic  vertigo  from  alcohol  or  tobacco  is  a  famiUar  type,  and 
to  the  toxic  class  we  may  also  refer  cases  produced  by  gastric 

'   Gentralblatt  fiir  Neurologic,  1902,  s.  565. 

^  Osterwald,  Neurologisches  Oentralblatt,  1906,  s.  265. 


170  NERVOUS    DISEASES 

disorder,  by  constipation,  and  by  some  cases  of  intestinal  parasites, 
though  in  the  last  instance  a  reflex  element  may  also  be.  present. 
Giddiness  is  often  present  in  neurasthenic  and  hysterical  patients, 
in  whom  it  may  be  ehcited  by  the  slightest  exciting  cause,  for 
example  by  rectal  examination. 

Ocular  vertigo  occurs  in  cases  of  paralysis  of  any  of  the  external 
ocular  muscles,  and  is  associated  with  diplopia.  The  visual  field 
being  erroneously  projected,  the  patient  judges  wrongly  as  to 
the  relation  of  his  body  to  what  he  sees.  "  Objects  appear  to  be 
in  certain  positions  where  the  patient's  feet,  as  a  matter  of  fact, 
fail  to  find  them  "  (Hughlings  Jackson).  The  giddiness  in  such 
cases  is  not  due  directly  to  the  diplopia,  for  it  persists  when  the 
sound  eye  is  covered.  The  condition  can  be  imitated  in  health  by 
closing  one  eye  and  displacing  the  other  eye  inwards  by  pressure 
with  the  finger,  when  if  the  subject  tries  to  walk  along  a  straight 
line  his  gait  becomes  very  unsteady. 

But  in  the  majority  of  cases  vertigo  is  associated  with  some 
disorder  of  the  ear.  It  may  result  from  wax,  or  foreign  bodies 
in  the  meatus,  or  it  may  supervene  during  ear-syringing,  especially 
if  there  be  a  perforation  of  the  drum.  The  pathological  cause  may 
also  lie  in  the  middle  ear,  as  in  otitis  media  or  obstruction  of  the 
Eustachian  tube,  or  the  condition  may  result  merely  from  sneezing 
or  blowing  the  nose,  also  from  spasm  of  the  tensor  tympani  muscle. 

Lastly,  there  is  what  is  laiown  as  Meniere's  disease,  or  laby- 
rinthine vertigo.  This  has  three  main  classes  of  symptoms : 
firstly,  giddiness  and  reefing,  due  to  affection  of  the  semicircular 
canals  ;  secondly,  deafness  and  tinnitus,  due  to  affection  of  the 
auditory  fibres  ;  and  thirdly,  associated  bulbar  phenomena,  such  as 
nausea  and  vomiting,  cardiac  failure,  cold  clammy  sweat,  &c.,  due 
to  affection  of  adjacent  medullary  centres. 

The  vertigo  of  Meniere's  disease  is  paroxysmal,  and  comes  on 
with  such  suddenness  that  the  patient  may  fall  to  the  ground  as 
if  struck  down  by  an  unseen  hand.  In  other  cases  he  reels,  but 
has  time  to  clutch  at  some  neighbouring  object  to  prevent  him- 
self from  falling.  The  giddiness  lasts  sometimes  for  hours ; 
shghter  attacks  may  pass  off  in  a  few  minutes.  It  is  increased 
by  movement,  and  the  sHghtest  attempt  to  raise  the  head  may 
induce  vomiting.  The  direction  in  which  the  patient  falls  is 
usually  forwards  or  towards  one  side,  and  commonly  away  from 
the  side  of  the  affected  ear.      Not  infrequently  nystagmoid  jerks 


CRANIAL  NERVES  171 

of  the  eyes  occur  during  the  attack,  and  double  vision  has  also 
been  observed.  The  vertigo  is  frequently  accompanied  or  followed 
by  headache,  nausea  and  vomiting,  lasting  sometimes  for  hours. 
Together  with  these  there  are  characteristic  auditory  phenomena, 
generally  a  sudc^en  loud  noise,  usually  unilateral.  There  is  also 
deafness,  more  or  less  complete,  on  the  same  side  as  the  tinnitus, 
with  dimmution  or  loss  of  bone-conduction.  A  certain  degree  of 
deafness  and  tinnitus  remains  between  the  attacks,  but  is  rarely 
absolute. 

Such  symptoms,  occurring  with  apoplectiform  suddenness, 
constitute  the  typical  picture  of  Meniere's  disease.  But  frequently 
the  paroxysms  are  much  slighter,  and  unassociated  with  nausea 
or  vomiting,  so  that  the  patient  may  simply  have  sudden  transient 
giddiness.  But  the  attacks  tend  to  recur  ;  rarely  does  a  patient 
escape  with  a  single  attack.  The  intervals  between  them  vary ; 
they  may  gradually  decrease  in  frequency,  or  may  progressively 
increase  until  after  successive  attacks  the  deafness  becomes 
absolute.     The  vertigo  then  usually  ceases. 

Labyrinthine  vertigo  is  distinguished  from  epileptic  vertigo  by 
the  coexistence  of  vertigo  with  tinnitus  and  deafness.  Loss  of 
consciousness,  which  is  the  rule  in  epilepsy,  is  rare  in  labyrinthine 
vertigo.  From  cerebral  haemorrhage  or  thrombosis  it  is  dis- 
tinguished by  the  presence  of  auditory  phenomena,  and  by  the 
absence  of  signs  of  a  focal  brain  lesion.  The  pathology  of  Meniere's 
syndrome  is  obscure.  Meniere  himself  described  a  haemorrhagic 
effusion  in  the  inner  ear.  But  as  Arthur  Cheatle  ^  has  lumin- 
ously suggested,  the  phenomena  are  in  many  respects  closely 
analogous  to  those  of  glaucoma,  and  may  possibly  be  due  to  a 
sudden  rise  of  tension  in  the  endolymph  or  perilymph,  whether 
produced  by  haemorrhage  or  other  causes  in  the  labyrinth  or  by 
sclerosis  of  the  middle  ear,  whereby  the  fenestra  ovalis  and  fenestra 
rotunda  become  fixed,  thereby  depriving  the  inner  ear  of  safety- 
valves  which  normally  permit  of  compensation  for  sudden  changes 
in  labyrinthine  pressure.  Labyrinthine  vertigo  often  yields  to 
bromides  or  to  small  doses  (^  to  1  grain)  of  quinine. 

A  focal  lesion  of  Deiters'  nucleus  produces  sudden  vertigo 
and  reeling,  together  with  nausea,  acute  distress,  transient  tinnitus 
or  deafness,  nystagmus,  and  sometimes  pain  in  the  distribution  of 
the  trigeminal  nerve      All  these  phenomena  are  easily  exphcable 

1  Archives  of  Otology,  vol.  xxvi.,  1897,  p.  185. 


172 


NBKVOUS    DISEASES 


when  we  remember  tlie  connection  of  Deiters'  nucleus  with  the 
cerebellum  and  with  the  oculomotor  nerves,  and  its  close 
proximity  to  the  sensory  nucleus  of  the  trigeminal. 

No  case  of  isolated  palsy  of  the  Ninth  or  Glosso-pharyngeal 
Nerve  has  yet  been  observed  in  man,  so  that  its  exact 
functions  are  not  completely  determined. 

We  know  that  it  supplies  taste-fibres  to  the  posterior  third  of  the 
tongue  and  to  the  soft  palate.  It  probably  also  supplies  the  taste 
buds  which  exist  on  the  epiglottis  and  on  the  arytenoid  cartilage.  The 
glosso-pharyngeal  is  also  a  nerve  of  common  sensation  for  the  back  of 
the  tongue,  part  of  the  soft  palate  and  upper  part  of  the  pharynx, 
whilst  it  has  motor  fibres  for  the  middle  constrictor  of  the  pharynx, 
and  for  the  stylopharyngeus. 


Fig.  78.— Paralysis  of  the  right  side  of  the  palate.  The  patient  is  saying 
"  Ah,"  and  the  palate  is  pulled  up  towards  the  left  side.  The  arrow 
points  to  the  centre  of  the  uvula. 

Paralysis  of  the  nerve  causes  ansesthesia  of  the  back  of  the 
tongue  and  pharynx,  difficulty  in  swallowing  and  deficient  taste 
in  the  posterior  third  of  the  tongue.  In  animals  when  this  nerve 
has  been  divided  experimentally,  the  pharynx  and  oesophagus 
remain  tonically  contracted,  owing  to  paralysis  of  the  "  autonomic  " 
inhibitory  fibres  contained  in  the  glosso-pharyngeal. 

The  Tenth  Nerve,  Vagus,  or  Pneumogastric  Nerve,  according 
to  modern  nomenclature,  is  held  to  include,  not  only  the  vagus 
itself  as  formerly  recognised,  but  also  those  roots  which  used  to 
be  called  the  "  bulbar  part  of  the  spinal  accessory."  Nowadays 
the  term  "  spinal  accessory  "  is  Hmited  to  the  spinal  part  of  the 
accessorius  which  arises  from  an  entirely  separate  nucleus,  whereas 
the  old  "bulbar  part"  is  derived  from,  and  belongs  to,  a  con- 
tinuation of  the  vagus  nucleus  (nucleus  ambiguus)  in  the  medulla. 

The  vagus  has  a  most  extensive  distribution.  It  contains  both 
cerebro-spinal  and  autonomic  fibres  and  supplies  the  pharynx,  larynx, 


CRANIAL   NERVES 


173 


oesophagus,  heart,  lungs,  stomach,  and  partly  even  the  intestines  and 
spleen.  By  its  auricular  branch  it  also  supplies  part  of  the  skin  of 
the  outer  ear.  Its  pulmonary  autonomic  fibres  are  motor  for  the 
bronchial  muscles  and  sensory  for  the  respiratory  passages.  The  vagus 
is  both  motor  and  sensory  for  the  oesophagus,  sensory  for  the  stomach, 
and  partly  motor  for  the  stomach  and  intestines.  Its  lowest  rcots  of 
origin  are  those  which  are  of  the  greatest  diagnostic  importance,  for 
they  contain  motor  fibres  for  the  levator  palati  and  the  larynx,  together 


Fig.  79. — Organic  laryngeal  paralyses  (Barwell). 

I.  Left  abductor  paralysis,  during  inspiration. 
II.  Left  abductor  paralysis,  during  phonation. 

III.  Left  recurrent  laryngeal  paralysis,  during  inspiration. 

IV.  Left  recurrent  laryngeal  paralysis,  during  phonation. 

with  autonomic  inhibitory  fibres  for  the  heart.  With  the  exception 
of  the  crico-thyroid  muscle,  which  is  innervated  by  the  superior  laryn- 
geal branch,  all  the  laryngeal  muscles  are  supplied  through  the  inferior 
or  recurrent  laryngeal  nerve. 

The  symptoms  of  vagus  paralysis  vary  according  to  the  site 
of  the  lesion.  Intra-cranial  lesions  may  affect  all  its  roots  of  origin, 
or  may  attack  the  upper  or  the  lower  roots  alone.  In  the  latter 
case  there  is  often  a  concomitant  affection  of  the  adjacent 
hypoglossal  nerve. 

If  the  whole  of  one  vagus  trunk  be  affected,  there  is  unilateral 
paralysis  of  the  palate  and  larynx  {Avellis's  syndrome),  together 


174 


NERVOUS    DISEASES 


with  anaesthesia  of  the  larynx  on  the  affected  side.  The  only  way 
to  recognise  a  unilateral  paralysis  of  the  palate  is  to  watch  the 
movement  of  its  median  raphe  when  the  patient  utters  a  long 
"Ah."  Normally  the  raphe  rises  straight  up.  But  if  one  side  of 
the  palate  be  paralysed,  the  healthy  side  alone  pulls  upwards  and 
the  raphe  deviates  to  the  sound  side,  forming  a  characteristic 
dimple  (Fig.  78). 

If  both  vagi  be  paralysed,  there  is  tachycardia  and  irregularity 
of  the  heart,  from  paralysis  of  the  cardio-inhibitory  fibres.     There 


FiGt.  80. — Functional  laryngeal  paralyses  (Barwell). 

V.  Adductor  paresis — all  the  adductors  affected — phonatlon. 
VI.  Adductor  paresis — arytenoideus  unaffected — phonation. 
VII.  Paralysis  of  the  thyro-arytenoidei— phonation. 
VIII.  Paralysis  of  the  arytenoideus — phonation. 

are  also  slowness  and  irregularity  of  respiration.  These  do  not 
occur  in  unilateral  vagus  palsy.  Gastric  symptoms  have  also 
been  observed  even  in  unilateral  cases,  such  as  gastric  dilatation, 
vomiting,  gastric  pain,  and  loss  of  the  sensations  of  hunger  and 
thirst. 

Of  all  these  symptoms,  the  most  constant  and  easiest  to 
recognise  are  the  affection  of  the  soft  palate  and  the  laryngeal 
palsy.  Paralysis  of  the  recurrent  laryngeal  nerve  may  occur 
alone.  The  commonest  cause  is  aortic  aneurism,  which  frequently 
compresses    the    nerve    on   the    left    side.      Mediastinal   growths 


CRANIAL    NERVES 


175 


may  also  compress  it,  or  its  paralysis  may  even  be  the  result 
of  mitral  stenosis,  when  the  left  auricle  becomes  dilated  and  thus 
compresses  the  nerve  directly  against  the  pulmonary  artery,  or  the 
auricle  may  force  the  left  bronchus  upwards  and  compress  the  nerve 
against  the  aortic  arch.^  In  recurrent  laryngeal  paralysis  the  vocal 
cord  on  the  affected  side  is  immobile,  fixed  in  the  cadaveric 
position,  i.e.  midway  between  abduction  and  adduction,  and  the 
voice  is  generally  hoarse  though  not  absent,  since  during  phonation 


Fig.  81. 


Fia.  81  A. 


Paralysis  of  right  spinal  accessory  nerve. 

Fig.  81  show.s  the  downward  and  outward  displacement  of  the  right  scapula.  Observe 
alteration  in  the  lateral  outlines  of  the  neck.  On  the  paralysed  side  the  outline  is 
formed  by  the  levator  anguli  scapulfe ;  on  the  normal  side  by  the  trapezius. 

Fig.  81 A  shows  the  patient  attempting  to  depress  the  head  against  resistance.  Oliserve  the 
absence  of  the  right  sterno-mastoid,  the  right  omo-hyoid  being  now  subcutaneous. 

the  healthy  cord  can  cross  the  middle  line  to  meet  the  paralysed 
one.  If  both  recurrent  laryngeals  be  paralysed,  both  vocal  cords  are 
motionless  and  in  the  cadaveric  position,  and  phonation  is  impossible 
since  the  cords  cannot  be  brought  together.  There  is  no  stridor 
except  on  deep  inspiration. 

It  is  here  convenient  to  recall  some  of  the  chief  diagnostic 
features  of  laryngeal  palsies  (Figs.  79  and  80).  Abductor  palsy, 
unilateral  or  bilateral,  is  always  organic,  and  is  often  the  earliest 
sign  of  a  commencing  recurrent  laryngeal  nerve  affection.     In  uni- 

1  Frischauer,  Wiener  Klin.  Wochenschrift,  Dec.  28,  1905. 


176  NERVOUS    DISEASES 

lateral  abductor  palsy  the  voice  is  unaffected,  but  on  laryngoscopic 
examination  the  paralysed  cord  is  seen  to  be  immobile  during 
inspiration,  not  moving  outwards  Hke  its  healthy  fellow.  On 
phonation  the  cords  meet  normally.  In  hilateral  abductor  palsy 
the  voice  is  also  unaffected,  since  both  cords  come  together  on 
phonation.  And  since  they  no  longer  move  outwards  during  in- 
spiration, but  on  the  contrary  are  sucked  together,  inspiration  is 
laboured  and  stridulous,  and  the  patient  is  in  danger,  since  the 
slightest  swelKng  of  the  cords  may  completely  block  the  glottis. 


Fjg.  82. — Paralysis  of  right  spiual  accessory  nerve,  showing  downward 
and  outward  displacement  of  scapula.  Owing  to  absence  of 
the  trapezius,  the  rhomboid  muscles  on  the  right  side  have  become 
subcutaneous. 

Paralysis  of  the  internal  thyro-arytenoid  muscle,  which  occurs  in 
some  cases  of  early  bulbar  paralysis,  is  characterised  by  an  oval 
instead  of  a  hnear  appearance  of  the  glottis  on  attempted  phona- 
tion, owing  to  loss  of  the  support  of  these  muscles.  The  voice  is 
therefore  hoarse,  but  abduction  and  adduction  are  otherwise 
unaffected.  Adductor  paralysis  is  always  bilateral  and  generally 
hysterical.  It  is  common  in  hysterical  aphonia.  The  patient 
loses  her  voice,  often  suddenly,  and  talks  in  a  whisper.  There 
is  no  stridor,  and  on  inspiration  the  cords  move  normally  out- 
wards. But  on  attempted  phonation  they  do  not  reach  the 
middle  hne.     The  condition  often  disappears  suddenly,  sometimes 


CRANIAL    NERVES 


177 


as  a  result  of  the  manipulations  of  laryngoscopy,  or  of  the  applica- 
tion of  strong  faradic  shocks  to  the  larynx. 

The  Eleventh  or  Spinal  Accessory  Nerve  is  distributed  to  the 
sterno- mastoid  and  to  part  of  the  trapezius.  It  is  exclusively  a 
motor  nerve.  When  it  is  paralysed,  we  have  paralysis  and  atrophy 
of  the  sterno-mastoid,  which  no  longer  stands  out  on  rotation  of 
the  head  to  the  opposite  shoulder,  nor  on  depressing  the  head  against 
resistance  (Figs.  81  and  81a).     The  sterno-mastoid  receives  a  small 


Fig.  S3.  Fig.  83^. 

Paraly.sis  of  right  spinal  accessory  nerve. 

Fig.  83. — Showing  position  at  rest. 
|Fig.  83A. — Showing  position  on  adduction  of  scapula;. 

part  of  its  innervation  from  the  second  cervical  nerve,  and  sometimes 
a  number  of  its  nmscle-fibres  survive  even  after  the  spinal  accessory 
is  divided.  The  paralysis  of  the  trapezius  varies  in  degree  accord- 
ing to  the  extent  to  which  the  muscle  is  supplied  by  the  spinal 
accessory  and  by  the  cervical  plexus  respectively.  Ordinarily  the 
uppermost  fibres  of  the  trapezius  are  innervated  by  the  spinal 
accessory,  whilst  the  middle  fibres  of  the  muscle  are  supplied 
by  the  third  and  fourth  cervical  nerves,  and  the  lowest  fibres 
of  all  by  the  spinal  accessory.  When  the  trapezius  is  paralysed, 
the  outline  of  the  neck   is  altered,  owing   to  the  levator  anguli 

M 


178  NERVOUS    DISEASES 

scapulse  having  become  subcutaneous,  and  there  is  a  characteristic 
deformity  of  the  angle  of  the  shoulder  resulting  from  the  displace- 
ment of  the  scapula  (Eig.  82).  The  scapula  on  the  paralysed  side 
is  displaced  downwards  and  outwards,  and  rotated  outwards,  so 
that  its  inner  border,  instead  of  being  parallel  with  the  spine,  is 
inclined  from  below  upwards  and  outwards.     When  the  patient 


Fig.  84. — Paralysis  of  right  hypoglossal  nerve  from  a  stab-wound  below 
the  jaw,  showing  atrophy  of  corresponding  half  of  tongue  and 
marked  deviation  to  the  right  when  protruded. 

braces  his  shoulders  back,  the  scapula  is  imperfectly  approximated 
to  the  middle  line,  and  the  rhomboids  on  the  paralysed  side  are 
visible  subcutaneously  (Figs.  .83  and  83a). 

The  Twelfth  or  Hypoglossal  Nerve  is  also  entirely  motor  in 
function. 

Immediately  after  its  exit  from  the  skull  it  receives  amongst  other 
connections  a  small  communicating  branch  from  the  cervical  sym- 
pathetic. The  hypoglossal  supplies  all  the  intrinsic  muscles  of  the 
corresponding  half  of  the  tongue.     Outside  the  skull  it  is  ioined  by 


CRANIAL    NERVES  179 

branches  from  the  first  and  second  cervical  nerves.,  and  from  these 
two  nerves  the  depressors  of  the  hyoid  bone  are  supplied,  through  the 
descendens  hi/poglossi. 

The  symptoms  of  hypoglossal  paralysis  are  very  characteristic 
(Fig.  84).  The  corresponding  half  of  the  tongue  is  atrophied 
and  wrinkled.  When  the  tongue  is  protruded  the  healthy  side 
causes  the  tip  to  be  pushed  round  to  the  paralysed  side  in  a  sickle- 
shaped  curve.     If  the  nerve  is  divided  suddenly,  by  accident  or 


Fig.  85. — Paralysis  of  spinal  accessory  and  hypoglossal  on  right  side,  showing 
downward  and  outward  displacement  of  right  shoulder,  also  atrophy 
of  right  half  of  tongue  with  deviation  to  the  right  on  protrusion. 

operation,  the  patient  feels  for  a  few  days  as  if  the  paralysed  half 
of  the  tongue  were  a  foreign  body,  interfering  with  articulation 
and  mastication.  But  this  sensation  soon  passes  off  as  the  patient 
becomes  accustomed  to  his  hypoglossal  palsy. 

If  the  lesion  of  the  hypoglossal  be  extra-cranial,  after  it  has 
received  the  small  communicating  branch  from  the  cervical 
sympathetic,  we  may  sometimes  observe  vaso-motor  changes  in  the 
atrophied  side  of  the  tongue.  In  two  of  my  cases  in  which  the 
twelfth  was  divided  intentionally  for  the  treatment  of  facial  palsy 
by  means  of  facio-hypoglossal  anastomosis,  the  tongue  was  pale 
on  the    paralysed  side.      From  unilateral  paralysis  of  the  hyoid 


180  NERVOUS    DISEASES 

depressors,  tlie  larynx  may  be  pulled  over  towards  the  sound 
side  during  swallowing. 

The  hypoglossal  nucleus  within  the  medulla,  as  we  have 
already  mentioned,  is  closely  connected  with  the  lowest  cells  of  the 
facial  nucleus,  viz.,  those  which  supply  the  orbicularis  oris. 
Hence  in  lesions  in  the  neighbourhood  of  the  hypoglossal  nucleus, 
the  muscles  of  the  lips  are  paralysed  together  with  those  of  the 
tongue.  This  weakness  of  lips  and  tongue  in  nuclear  lesions  is 
generally  bilateral,  owing  to  the  close  proximity  of  the  hypoglossal 
nuclei  to  the  middle  line. 

Intra-cranial  lesions  of  the  hypoglossal  nerve,  e.g.  from  a  patch 
of  syphilitic  meningitis,  very  frequently  involve  other  cranial  nerves 
in  the  neighbourhood.  One  of  the  commonest  multiple  palsies 
is  that  which  produces  Hughlings-Jacksoyi's  syndrofne,  viz., 
hemiatrophy  of  the  tongue,  paralysis  of  the  trapezius  and  sterno- 
mastoid,  and  paralysis  of  the  vocal  cord  and  soft  palate,  all  on 
the  same  side  (Fig.  85).  This  is  the  result  of  a  lesion  implicating 
the  twelfth,  the  eleventh,  and  the  lowest  roots  of  the  tenth  nerve. 


CHAPTER   XI 

PAIN   AND   OTHER   ABNORMAL   SUBJECTIVE   SENSATIONS 

There  is,  perhaps,  no  symptom  for  which  we  are  more  frequently 
consulted  than  that  of  pain.  For  its  satisfactory  treatment  the 
underlying  cause  must  first  be  determined — sometimes  no  easy 
matter. 

With  the  exception  of  cases  in  which  pain  arises  in  a  healthy 
individual  from  some  unduly  violent  stimulus,  pain  is  always  patho- 
logical. The  vast  majority  of  pains  are  due  to  irritation  of  some 
peripheral  sensory  nerve  or  of  a  posterior  root.  Less  commonly 
pain  may  be  due  to  abnormal  sensitiveness  of  the  cortical  centres, 
and  is  functional  in  origin.  Stimulation  of  the  surface  of  the  brain 
gives  rise  to  no  pain,  but  the  meninges  are  exquisitely  sensitive, 
the  cerebral  membranes  being  innervated  by  the  trigeminal  nerve. 
Intra-cranial  diseases  therefore  probably  cause  pain  chiefly  through 
the  intermediation  of  the  sensitive  meninges.  It  is  possible,  how- 
ever, that  the  pain  in  some  cases  of  syringomyelia  may  not  be 
of  meningeal  origin,  but  due  to  actual  distension  of  the  syringo- 
myehc  cavity  by  the  fluid  within,  though  against  this  view  is  the 
fact  that  pain  is  a  late  phenomenon  in  this  disease. 

Spontaneous  sensations  of  discomfort  vary  in  degree  and  in 
kind.  Milder  varieties,  not  amounting  to  actual  pain,  are  classed 
as  dyssesthesise.  They  include  such  symptoms  as  spontaneous 
tingling,  "  pins  and  needles,"  dulness,  itching,  flushing,  &c.,  whilst 
among  the  more  severe  varieties  are  the  intense  and  agonising 
pains  of  tic  douloureux,  angina  pectoris,  renal  or  biliary  colic,  or 
the  lightning-pains  of  tabes. 

In  the  diagnosis  of  the  cause  of  any  particular  dyseesthesia  or 
pain,  there  is  one  invariable  rule  which  we  should  always  follow, 
namely,  to  make  a  careful  local  examination  of  that  part  of 
the  body  to  which  the  abnormal  sensation  is  referred.  Only  in 
this  way  can  we  escape  gross  errors,  such,  for  example,  as  that  of 
mistaking  the  pain  of  herpes  zoster  for  that  of  pleurisy.  In 
every  local  pain  we  should  first  search  for  a  local  cause,  whether 

181 


182  NERVOUS    DISEASES 

in  the  skin,  muscles,  bones,  joints,  glands,  or  other  subjacent 
structures.  Pain  due  to  local  disease  is  usually  more  or  less 
continuous,  and  accompanied  by  objective  phenomena  such  as 
redness  of  the  skin,  swelling  or  tenderness  of  the  diseased  tissues, 
rigidity  of  joints,  and  so  on.  The  painful  cramps  of  tetanus, 
rabies,  and  strychnia-poisoning  are  easily  recognised  and  need 
not  be  further  described. 

Some  pains  are  generalised  all  over  the  body,  for  example,  the 
pains  of  acute  illnesses  such  as  influenza,  smallpox,  and  other 
fevers  of  rapid  onset.  In  such  cases  the  elevation  of  tempera- 
ture, the  presence,  perhaps,  of  a  rash,  and  usually  the  occurrence 
of  other  similar  cases  in  epidemic  form,  all  help  us  in  the 
diagnosis. 

Intractable  paroxysmal  pains  of  hemiplegic  distribution,  in  the 
face,  trunk  and  limbs,  so-called  hemiplegia  dolorosa,  are  highly 
suggestive  of  a  lesion  localised  in  the  optic  thalamus.^  In  such 
thalamic  lesions  there  is  also  hemi-ansesthesia  of  the  affected 
limbs  and  face,  hemi-hypersesthesia  to  temperature  and  pin-pricks, 
together  with  spontaneous  choreiform  or  athetoid  movements  and 
also  hemi-ataxy  on  voluntary  movement.  These  cases  of  hemi- 
plegia dolorosa  must  be  carefully  distinguished  from  the  joint 
pains  which  are  not  uncommon  in  ordinary  chronic  hemiplegia, 
which  are  due  to  secondary  arthritic  changes  and  are  usually 
alleviated  by  massage,  hydro -therapeutics  and  anti-rheumatic 
remedies. 

Most  cases  of  pain  or  discomfort,  however,  are  localised  to 
some  more  definite  area,  and  therefore  for  diagnostic  purposes 
the  most  convenient  plan  of  studying  pains  and  other  subjective 
sensations  is  by  considering  the  different  paros  of  the  body  in  turn. 
Headache. — Cephalalgia. — ^A  diagnosis  of  "  headache  "  alone 
is  never  sufficient.  Headache  is  not  a  disease,  but  merely  a 
symptom. 

When  a  patient  complains  of  headache,  local  causes  should 
first  of  all  be  excluded.  Amongst  the  commonest  local  extra-cranial 
causes  we  should  bear  in  mind  rheumatic  myositis  of  the  occipito- 
frontalis  muscle,  with  its  characteristic  tenderness  on  brushing  the 
hair,  with  aggravation  of  pain  on  movement  of  the  scalp,  and 
with  scattered  areas  of  nodular  induration  in  the  muscle-fibres, 
recognisable  on  careful  palpation  and  exquisitely  tender  on  light 

^  Dejarine  and  Roussy,  Revue  neurologique,  1906,  No.  12. 


PAIN  183 

pressure.  Deep  pressure,  on  the  other  hand,  often  relieves  the 
pain.  Meanwhile  we  usually  find  a  considerable  degree  of  rigidity 
in  the  muscles  of  the  neck.  This  headache  is  often  relieved 
promptly  by  hot  applications  and  by  massage.  Erysipelas  is 
accompanied  by  local  redness,  heat  and  oedema,  and  by  fever. 
Periostitis  of  the  pericranium  causes  tenderness  on  pressure  and  is 
often  syphilitic  in  origin,  in  which  case  the  pain  is  commonly  worse 
at  nights. 

Headaches  from  local  causes  in  the  cranial  bones  are  most 
commonly  due  to  inflammation  of  the  mucous  membrane  lining  the 
various  air-cells,  e.g.  the  mastoid,  frontal,  or  ethmoidal  cells,  or  even 
to  an  ordinary  coryza.  Here  the  previous  history  of  the  case, 
together  with  the  local  examination,  will  serve  to  ind  cate  the 
cause.  Less  frequently  caries  of  the  bones  or  local  exostoses 
may  be  present.  Carious  teeth  often  cause  headache,  referred 
especially  to  the  temporal  region. 

Gross  intra-cranial  disease  may  produce  intense  headache,  either 
from  local  affection  of  the  meninges  as  in  the  various  forms  of 
meningitis  (syphilitic,  tuberculous,  or  pyogenic),  or  from  general 
increase  of  intra-cranial  pressure,  as  in  diffuse  meningitis,  intra- 
cranial abscess,  gumma,  or  tumours.  Headaches  of  intra-cranial 
origin  are  nearly  always  paroxysmal,  or  if  there  be  a  continuous 
pain,  it  has  paroxysmal  exacerbations.  These  headaches  are  often 
associated  with  the  other  classic  signs  of  increased  intra-cranial 
pressure,  especially  with  nausea,  vomiting,  and  optic  neuritis. 
In  every  case  of  obscure  headache  we  should  make  a  careful 
ophthalmoscopic  examination.  The  position  of  the  headache  does 
not  necessarily  correspond  with  that  of  the  tumour.  Tumours  of 
the  posterior  fossa  produce  the  most  severe  headache. 

Then  there  are  the  headaches  which  result  from  abnormahties 
of  the  intra-cranial  circulation,  especially  from  arterial  hypersemia, 
as  in  renal  disease  or  in  suppressed  menstruation,  or  temporarily 
from  drugs  such  as  nitrite  of  amyl,  erythrol  tetranitrate,  or  alcohol. 
Hypersemia  produces  a  throbbing  pain,  sometimes  associated  with 
giddiness,  tinnitus,  affection  of  vision,  and  a  tendency  to  attacks 
of  epistaxis.  The  venous  hypera^mia  of  severe  cardiac  disease  or 
of  emphysema  may  also  produce  headache,  which  is  aggravated 
by  coughing.  The  headache  of  anaemia  is  probably  mainly  toxic 
in  origin,  rather  than  due  to  actual  deficiency  in  the  supply  of  blood 
to  the  head. 


184  NEEVOUS  DISEASES 

Certain  cases  of  hemiplegia  are  preceded,  for  days  or  even 
weeks,  by  headache.  This  is  sometimes  present  in  cerebral  throm- 
bosis (encephalomalacia),  where  a  premonitory  headache  is  of  con- 
siderable diagnostic  value.  Still  more  frequently,  the  onset  of  a 
cerebral  hcemorrhage  is  accompanied  by  headache.  Therefore  if  an 
elderly  man  complains  of  headaches  and  bleeding  from  the  nose, 
we  should  be  cautious  in  checking  epistaxis  which  may  act  as  a 
safety-valve,  and  may  save  him  from  an  attack  of  cerebral  haemor- 
rhage.   Cerebral  embolism  is  not  usually  associated  with  headache. 

There  is  another  group  of  headaches  which  are  produced  by 
peripheral  irritation  in  various  parts  of  the  body.  Thus,  for 
example,  visceral  irritation  may  cause  headache,  often  accompanied 
by  areas  of  superficial  tenderness,  as  in  ovarian  or  uterine  diseases, 
or  in  the  headaches  from  which  so  many  women  suffer  at  the 
menstrual  periods,  and  frequently  also  throughout  the  menopause. 
Head  has  pointed  out  that  the  different  viscera  have  special  areas 
of  superficial  tenderness,  temporal,  vertical,  or  occipital.  In  some 
people  the  swallowing  of  an  ice  causes  sudden  frontal  headache, 
when  the  ice  reaches  the  oesophagus  or  stomach.  This  is  a 
typical  "  reflex  "  gastric  headache.  Every  autumn  we  come  across 
cases  of  "  gun  headache "  amongst  sportsmen,  not  simply  the 
result  of  the  auditory  stimulus  of  the  noise  of  the  gun,  but  due 
partly  to  the  shock  of  repeated  recoils  of  the  weapon.  Orbital 
headaches  are  fairly  frequent,  sometimes  the  result  of  disease  such 
as  glaucoma  or  iritis,  but  much  more  commonly  arising  from  errors 
of  refraction,  especially  hypermetropia  and  astigmatism.  Even 
apart  from  this,  headache  may  result  from  prolonged  eye-strain, 
e.g.  after  sight-seeing  in  picture-galleries,  being  commoner  in 
people  who  have  some  error  of  refraction. 

A  large  group  of  headaches  are  toxic  in  origin,  the  toxins 
altering  the  intra-cranial  circulation,  usually  in  the  direction  of 
raising  the  blood-pressure.  The  onset  of  certain  infective  fevers 
is  associated  with  headache,  for  example  in  smallpox  and  influenza 
(commonly  associated  with  pain  in  the  back),  in  enteric  fever 
associated  with  dyspeptic  symptoms,  in  scarlatina,  pneumonia,  &c. 
In  such  cases  the  temperature,  the  characteristic  rash,  and  the 
other  signs  and  symptoms  will  guide  us.  Poisoning  by  toxic 
substances  is  also  the  main  cause  of  the  headache  of  dyspepsia, 
whether  it  be  the  well-known  "  Katzen- jammer " — the  bursting 
morning-headache  and  nausea  following  a  joyous  alcoholic  evening 


PAIN  185 

(this  headache,  by  the  way,  can  often  be  relieved  by  a  20-grain 
dose  of  calcium  lactate),  or  the  headache  of  chronic  dyspepsia 
especially  when  associated  with  a  constipated  intestine.  Headache 
also  results  from  poisoning  with  carbonic  oxide,  carbonic  acid 
and  other  respiratory  sewage  in  ill-ventilated  rooms  or  at  crowded 
meetings.  Other  poisons,  again,  are  autogenetic  in  origin,  as  are 
the  headaches  of  gout,  urasmia  and  diabetes.  The  typical  renal 
headache  is  occipital  in  situation,  although  it  may  also  occur  in 
the  frontal  or  temporal  regions. 

Sunstroke  causes  acute  diffuse  headache.  Severe  cases  are 
often  accompanied  by  other  symptoms  such  as  delirium,  hyper- 
pyrexia and  coma,  together  with  pleocytosis  of  the  cerebro-spinal 
fluid.  Neurasthenia  and  exhaustion,  whether  from  overwork,  from 
excessive  study  or  from  other  excesses,  are  often  associated  with 
headache,  frontal,  occipital,  or  circular,  feeling  like  a  tight  elastic 
band  {douleur  en  casque).  The  post- epileptic  headache  following 
a  fit  is  sometimes  severe  and  may  be  associated  with  vomiting. 

Bilateral  headaches  are  most  commonly  toxic.  The  headache 
of  dyspepsia  is  usually  referred  to  the  frontal  region,  that  of 
constipation  to  the  occiput,  whilst  vertical  headaches  are  most 
commonly  due  to  anaemia  or  to  debihty.  Some  cases  of  con- 
cussion of  the  brain  are  followed  by  obstinate  headaches,  recur- 
ring for  many  months.  These,  I  believe,  may  be  partly  toxic 
in  origin,  a  smaller  amount  of  toxin  being  efficient  in  producing 
headache  after  concussion  than  in  the  case  of  a  healthy  individual, 
whilst  in  other  instances  the  headaches  occur  on  sHght  mental 
exertion,  especially  where  the  patient  has  been  allowed  to  return 
to  work  prematurely.  Hence  the  importance  of  complete  physical 
and  mental  rest  after  a  severe  head  injury,  even  in  the  absence 
of  signs  of  an  organic  lesion. 

Most  of  the  headaches  to  which  we  have  referred  are  bilateral 
or  mesial  in  situation.  Let  us  now  consider  a  different  group — 
the  unilateral  or  circumscribed  pains. 

Sometimes  these  are  due  to  local  disease  of  the  scalp,  peri- 
cranium or  skull,  in  which  case  local  examination  will  generally 
reveal  the  cause.  Or  they  may  result  from  intra-cranial  disease, 
for  example,  meningitis,  abscess,  gumma  or  tumour.  If  the  under- 
lying disease  be  near  the  surface  of  the  skull,  the  site  of  the  pain 
sometimes  corresponds  with  that  of  the  disease.  But  this  is  by 
no  means  always  the  case.     I  remember  a  striking  case  of  right- 


186  NERVOUS    DISEASES 

sided  cerebellar  tumour  in  which  the  pain  was  confined  to  the  left 
supraorbital  region.  The  growth  was  diagnosed  and  successfully 
removed. 

Some  headaches  are  associated  with  great  pallor  of  the  face 
— apparently  due  to  vaso-motor  spasm  of  the  cerebral  vessels,  often 
relieved  by  inhalation  of  amyl  nitrite.  Others  are  associated 
with  arterial  hypersemia,  throbbing  arteries,  and  a  flushed  face. 
These  are  sometimes  promptly  relieved  by  compression  of  the 
carotid  artery  on  the  corresponding  side.  Such  angio-neurotic 
headaches  are  rarely  bilateral. 

A  very  acute  circumscribed  variety  of  headache  is  known 
as  the  clavus  hystericus,  an  agonising  pain  usually  referred  to  the 
vertex,  as  if  a  nail  were  pressing  into  the  brain.  It  occurs  in 
certain  cases  of  hysteria  and  neurasthenia.  It  is  unassociated  with 
any  other  evidences  of  intra-cranial  disease,  and  its  very  intensity 
leads  us  to  a  suspicion  of  its  true  nature. 

The  pain  of  sick-headache  or  migraine  (hemicrania),  with  its 
paroxysmal  attacks  recurring  at  intervals  of  days  or  weeks,  the 
patient  during  the  intervals  being  free  from  headache,  is  usually 
easy  of  recognition.  The  duration  of  each  paroxysm  varies  from 
a  few  hours  to  one  or  two  days.  Most  cases  begin  in  the  morning 
and  last  till  the  same  evening.  Migraine  is  a  family  disease  which 
generally  appears  in  childhood  and  recurs  throughout  the  strenu- 
ous period  of  life,  tending  to  disappear  in  old  age.  The  pain  of 
migraine  is  often  alleviated  by  pressure  on  the  common  carotid 
artery  of  the  corresponding  side,  but  reappears  when  the  pressure 
is  removed.  It  is  not  uncommon  to  have  unilateral  vasomotor 
changes  during  the  attack.  Thus  the  face  and  ear  may  be  flushed 
on  the  affected  side.  The  pupils  may  also  become  temporarily 
unequal,  although  this  is  by  no  means  constant.  Migrainous 
headache  generally  culminates  in  vomiting,  and  is  sometimes 
preceded  by  a  visual  aura  in  the  form  of  a  scintillating  scotoma, 
consisting  of  a  bhnd  area  in  one  half  of  the  visual  field  (usually, 
but  not  always,  on  the  side  opposite  to  that  of  the  unilateral 
headache).  The  blind  area  is  bounded  at  its  periphery  by  a 
luminous  zig-zag  coloured  spectrum.  This  scotoma  not  infre- 
quently develops  into  a  temporary  total  hemianopia.  The  head- 
ache of  migraine  is  generally  unilateral,  and  is  referred  to  the 
front  part  of  the  head  on  the  side  contra-lateral  to  that  of  the 
visual  phenomena.     Thus  if  the  visual  sensations  are  in  the  left  side 


PAIN  187 

of  the  visual  fields,  the  headache  is  generally  right-sided,  and  vice 
versd.  Less  commonly  a  migrainous  attack  may  be  preceded  by  a 
non-visual  aura  of  some  sort,  e.g.,  by  a  subjective  sensation  of 
tingling  in  one  hand  spreading  slowly  up  the  arm  to  the  face  and 
tongue,  and  followed  by  headache  on  the  opposite  side  of  the  head. 
If  the  tingling  be  right-sided  there  may  be  slight  transitory  aphasia. 
This  variety  of  migraine  is  distinguished  from  a  minor  epilepti- 
form attack  by  the  greater  intensity  and  unilateral  limitation  of 
the  migrainous  headache,  by  the  slow,  deliberate  march  of  the 
migrainous  aura,  lasting  perhaps  for  many  minutes,  by  the  absence 
of  unconsciousness,  by  the  absence  of  clonic  movements,  and  by 
the  fact  that  the  premonitory  tingling  of  migraine  may  spread 
bilaterally  to  the  tongue  and  lips,  whereas  in  an  epileptiform 
attack,  if  the  aura  spreads  to  the  tongue  or  face,  it  remains  uni- 
lateral.^ Migraine  and  epilepsy  may  alternate  in  the  same 
patient.  Migraine  ophtalmoplegique  is  a  rarer  variety,  in  which, 
in  addition  to  hemicranial  pain,  there  is  transient  paralysis  of  the 
third  nerve  on  the  same  side  as  the  headache,  with  ptosis,  external 
strabismus,  mydriasis,  &c. 

We  now  pass  to  pains  in  the  region  of  the  trigeminal  nerve. 
Of  these  tic  douloureux  is  the  most  agonising  pain  from  which 
a  patient  can  suffer.  The  pain  rarely  attacks  all  three  divisions 
of  the  nerve,  but  is  usually  confined  to  one  division  (especially 
the  supraorbital),  or  it  may  attack  two  adjacent  divisions.  The 
disease  is  hardly  ever  bilateral  except  in  cases  of  diabetes.  The 
patient  has  paroxysms  of  intolerable  agonising  pain  in  the  area 
of  the  affected  division.  During  the  attack,  the  face  is  often 
thrown  into  strong  involuntary  tonic  spasm  on  the  affected  side, 
there  is  excessive  lachrymation,  and  sometimes  secretion  of  nasal 
mucus  and  saliva,  all  on  the  affected  side.  Not  only  do  paroxysms 
occur  spontaneously,  but  the  slightest  stimuli  often  suffice  to 
induce  an  attack,  and  therefore  the  patient  avoids  chewing  food 
on  the  affected  side.  I  have  known  cases  in  which  it  was  impossible 
for  the  patient  to  wash  his  face  for  weeks  at  a  time,  lest  an  attack 
should  be  thereby  precipitated.  Inveterate  trigeminal  neuralgia 
sometimes  drives  the  patient  to  suicide. 

Apart  from  these,  there  are  numerous  varieties  of  more  locahsed 
paroxysmal  neuralgic  pains  referred  to  individual  branches  of  the 
trigeminal  nerve,  and  associated  with  "  tender  points  of  Valleix  " 

^  Gowers,  British  Medical  Journal,  Dec.  3,  1906. 


188  NERVOUS    DISEASES 

over  their  foramina  of  exit.  In  such  local  neuralgias,  and  in  tic 
douloureux  itself,  we  should  always  search  carefully  for  some  local 
exciting  cause  in  the  mouth,  nose,  ear,  or  eye.  A  carious  or  inflamed 
tooth  may  cause  neuralgia  in  the  whole  of  the  corresponding 
division  of  the  fifth  nerve,  and  the  dental  surgeon  by  extracting  it 
will  reheve  the  condition.  But  we  must  beware  of  extracting  sound 
teeth  simply  because  the  patient  refers  neuralgic  pain  to  them. 
Sometimes  an  abnormally-placed  tooth,  though  healthy  in  itself, 
may  cause  neuralgia.  Thus  a  lady  of  fifty- eight  had  had  a  constant 
burning  pain  along  the  right  side  of  her  tongue  for  eight  years, 
together  with  a  feehng  of  numbness  in  the  area  of  the  second  divi- 
sion of  the  fifth  nerve.  This  had  been  vainly  treated  by  numer- 
ous drugs,  whilst  all  the  time  the  real  exciting  cause  lay  in  an 
imperfectly-erupted  lower  wisdom-tooth  on  the  corresponding 
side,  the  date  of  the  pain  coinciding  with  the  first  appearance  of 
the  tooth.  Disease  of  the  antrum  or  other  accessory  air- 
sinus,  nasal  polypi,  and  other  local  lesions  may  all  cause 
localised  neuralgias.  If,  in  addition,  the  patient  be  anaemic 
or  gouty,  the  tendency  to  neuralgia  is  increased.  But  ansemia 
or  gout  alone  will  not  cause  a  local  neuralgia.  Some  local 
determining  cause  must  also  be  present,  though  it  is  some- 
times difficult  to  discover.  The  combination  of  unilateral  pain  in 
the  region  of  the  third  division  of  the  trigeminal  with  obstructive 
deafness  of  the  Eustachian  tube  type,  and  impaired  movement  of 
the  soft  palate  on  the  same  side,  is  generally  due  to  a  new  growth 
in  the  lateral  wall  of  the  naso-pharynx.i  Syphihtic  basal  menin- 
gitis or  gumma,  impHcating  the  fifth  nerve  in  the  floor  of  the  skull, 
may  cause  trigeminal  neuralgia.  The  patients  usually  show  other 
evidences  of  intra-cranial  disease,  and  we  should  look  for  signs  of 
involvement  of  the  sensory  or  motor  root  (see  page  154).  If  such 
lesions  last  any  considerable  time,  they  tend  to  produce  some 
anaesthesia  of  the  affected  nerve-area.  Localised  anaesthesia, 
suggests  an  organic  neuritis  rather  than  a  mere  neuralgia. 

Let  us  now  consider  the  various  pains  which  may  be  met  with 
in  the  trunk.  Firstly,  there  are  the  various  root-pains,  due 
to  irritation  of  the  corresponding  posterior  root  or  roots  in  the 
affected  area.  Sometimes  such  root  irritation  is  due  to  disease 
of  the  spinal  meninges  (tubercle,  syphilis,  or  tumour),  to  osteo- 
arthritis, caries  or  tumours  of  the  spinal  column,  or  to  intra-thoracic 

1  Trotter,  Brit.  Med.  Journal,  Oct.  28,  1911. 


PAIN  189 

aneurisms  and  new  growths.  Bone  pains  in  the  spine  are  associated 
with  local  tenderness  and  rigidity.  If  we  see  a  patient  supporting 
his  head  with  both  hands  owing  to  pain  in  the  neck,  this  is  almost 
pathognomonic  of  disease  of  the  cervical  vertebrae.  Root-pain 
commencing  unilaterally  and  later  becoming  bilateral  is  practically 
pathognomonic  of  a  tumour  of  the  spinal  meninges.  These  pains, 
when  due  to  organic  lesions  of  the  roots,  are  not  infrequently 
associated  with  a  degree  of  hyperaesthesia  or  anaesthesia  of  the 
painful  area — ancesthesia  dolorosa.  If  the  spinal  cord  be  com- 
pressed or  infiltrated  by  the  same  lesion  as  that  which  im- 
phcates  the  posterior  roots,  we  have  evidence  of  sensory  or 
motor  paralysis  of  the  parts  below  the  lesion,  with  the  usual 
changes  in  the  reflexes,  &c.  The  girdle-pains  of  tabes  are  due 
to  affection  of  the  corresponding  posterior  roots.  Tabetic  girdle- 
pains  vary  in  degree  from  the  sensation  of  a  narrow  constrict- 
ing cord  to  one  of  a  broad  cuirass  enveloping  a  large  part  of  the 
trunk.  Such  a  cuirass  often  feels  incomplete  either  in  front  or 
behind  (Fig.  90,  p.  212).  Root-pains  may  also  occur  in  some 
cases  of  disseminated  sclerosis  {sclerosis  multiplex  dolorosa),  and 
unless  this  fact  be  borne  in  mind  a  false  diagnosis  of  spinal  tumour 
may  be  made.^  Another  root-pain  is  that  associated  with  herpes 
zoster,  which  is  a  disease  of  the  posterior  root-ganglion.  Herj^etic 
pain  is  practically  always  unilateral,  and  may  either  precede  or 
succeed  the  eruption  of  the  herpetic  vesicles.  It  may  last  for 
months  after  the  vesicles  have  disappeared.  The  pain  of  herpes 
is  often  so  sharp  that  it  may  be  mistaken  for  that  of  pleurisy,  from 
which  it  is  distinguished  by  auscultation.  Herpes  zoster  is  often 
accompanied  by  a  lymphocj^osis  of  the  cerebro -spinal  fluid. 
Pleurodynia  is  a  pain  in  one  or  more  intercostal  spaces,  due  to 
a  "  rheumatic  "  myalgia  of  some  of  the  intercostal  muscles.  It 
somewhat  resembles  the  pain  of  pleurisy,  but  is  easily  distinguished 
by  the  normal  temperature  and  by  the  absence  of  friction-sounds 
on  auscultation.  There  is  also  a  very  common  trunk-pain  which 
we  meet  with  in  people  who  are  neuiasthenic  or  debihtated.  It 
is  a  deep  boring  pain,  usually  below  the  inferior  angle  of  one  or 
other  scapula.  It  is  more  diffuse  and  less  superficial  than  the 
pain  of  herpes,  and  it  has  none  of  the  physical  signs  of  pleurisy 
or  pleurodynia.  The  pain  of  traumatic  neurasthenia,  especially 
after    a     railway    or    other    accident    ("  railway     spine "),    may 

^  Frankl-Hochwarfc,  Neurologisches  Gentralhlatt,  1906,  s.  973. 


190  NERVOUS    DISEASES 

simulate  that  of  organic  spinal  lesions,  especially  when  a 
hysterical  paraplegia  coexists.  But  the  diagnosis  can  usually 
be  made  by  noting  the  excessive  hyperaesthesia  of  the  spine,  the 
absence  of  signs  of  organic  disease  and  the  presence  of  various 
hysterical  "  stigmata  "  (see  later,  p.  389).  Mammary  neuralgia 
or  mastodynia  also  occurs  in  hysterical  and  neurasthenic  patients, 
and  must  be  distinguished  from  disease  of  the  gland  by  means  of 
physical  examination. 

We  have  also  to  bear  in  mind  the  various  reflected  fains 
which  may  occur  in  visceral  diseases.  Thus,  for  example,  in 
pericarditis  there  may  be  precordial  or  epigastric  pain.  Physical 
examination  will  clear  up  the  diagnosis  in  cases  of  aneurism 
and  of  mediastinal  growths. 

Phrenic  neuralgia  is  of  considerable  clinical  interest.  It  should 
be  borne  in  mind  that  the  phrenic  is  a  mixed  nerve,  supplying  not 
only  diaphragmatic  motor  fibres  but  also  sensory  fibres  to  the 
diaphragm,  to  the  extra-pleural  and  extra-peritoneal  connective 
tissues,  and  to  the  supra-renal  body  of  the  corresponding  side.  In 
addition,  the  right  phrenic  supplies  the  liver  and  its  sub-peritoneal 
covering,  also  the  inferior  vena  cava  and  the  right  auricle.  The 
phrenic  nerve  has  various  connections  with  spinal  and  splanchnic 
nerves,  notably  with  the  inter- vertebral  ganglia  of  the  lower  cervical 
posterior  roots  ^  (from  the  third  to  the  sixth  cervical).  Thus  in 
certain  diseases  such  as  diaphragmatic  pleurisy,  gall-stones,^ 
hepatic  abscess,  supra-renal  tumours,^  &c.,  we  may  have  reflected 
pain  in  the  region  of  the  corresponding  shoidder,  often  accompanied 
by  cutaneous  hypersesthesia. 

One  of  the  most  severe  of  all  trunk  pains  is  the  well-known 
angina  pectoris.  This  is  a  paroxysmal  suffocative  pain,  or  feeling 
of  intolerable  oppression  in  the  region  of  the  heart,  often  radiating 
down  one  or  both  arms,  but  especially  down  the  left  arm.  To- 
gether with  this,  there  is  a  sensation  of  impending  death.  It  is 
commonest  in  male  patients  at  or  after  middle  life,  and  is  usually, 
though  not  invariably,  associated  with  evidence  of  vascular  degene- 
ration. It  has  to  be  distinguished  from  toxic  or  neuralgic  angina, 
so-called  "  pseudo-angina,"  a  similar  but  much  less  serious  affec- 
tion, met  with   most  commonly  in  young  girls,  in  women  who 

^  Kidd,  Rev.  of  Neurol,  and  Psych.,  1911,  p.  587. 

^  Mackenzie,  Brain,  1893,  p.  339  ;  also  Symptoms  and  their  Interpretation, 
1909,  p.  45. 

3  Mayo  Robson,  Brit.  Med.  Journal,  1899,  vol.  ii.  p.  1180. 


PAIN  191 

have  been  lactating  too  long,  or  in  patients  before   middle   life 
who  smoke  tobacco  or  drink  tea  to  excess. 

Irritation  of  the  sensory  nerves  at  the  gastric  end  of  the 
oesophagus,  by  abnormal  acids  or  other  irritants  in  the  stomach, 
may  cause  burning  pain,  usually  referred  to  the  seventh  left 
chondro-sternal  junction,  and  sometimes  also  to  the  left  inter- 
scapular region.  Such  pains  are  associated  with  other  dyspeptic 
symptoms  to  which  we  need  not  here  refer  further.  As  regards  the 
situation  of  reflected  pains  in  diseases  of  various  parts  of  the  gastro- 
intestinal tract,  it  is  useful  to  bear  in  mind  Mackenzie's  rule,^  that 
pain  due  to  affections  of  the  digestive  tract  is  referred  across  the 
middle  line  of  the  abdomen,  in  regularly  descending  areas  as  we  pass 
from  the  stomach  towards  the  large  intestine.  Thus  the  epigastrium 
is  the  region  for  gastric  pains  (disease  at  the  cardiac  end  causing 
pain  higher  up  than  pyloric  affections),  the  umbilical  area  is 
the  region  for  pains  of  the  small  intestine,  the  hypogastric  area 
the  site  of  pains  due  to  the  large  intestine.  A  striking  experi- 
mental corroboration  of  this  can  be  obtained  at  any  time  by 
taking  a  sharp  purgative  drug.  When  the  familiar  colicky  pains 
appear,  they  are  felt  first  in  the  region  of  the  umbilicus,  but  soon 
they  descend  lower  and  lower,  and  when  they  arrive  close  above 
the  pubes,  the  call  for  evacuation  of  the  bowel  becomes  "  urgent 
and  imperative." 

To  discuss  fully  the  various  causes  of  acute  abdominal  pain 
would  require  many  chapters  of  description.  We  have  to  bear 
in  mind  not  only  diseases  of  the  gastro-intestinal  tract,  in  the 
form  of  catarrh,  ulcer,  muscular  spasm,  &c.,  but  also  perforations 
of  various  hollow  viscera,  the  stomach,  gall-bladder,  intestines 
(including  the  vermiform  appendix),  rupture  of  a  pyo-salpinx 
or  of  a  tubal  pregnancy,  biliary  or  renal  colic,  acute  pancreatitis, 
torsion  of  an  ovarian  pedicle,  &c.  In  every  instance,  not  only 
should  we  carefully  examine  the  whole  abdomen,  but  we  should, 
if  necessary,  examine  the  pelvis,  per  rectum  or  fer  vaginam,  and 
investigate  the  urine  and  dejecta. 

Apart  from  acute  renal  colic,  a  floating  kidney  is  a  fairly  common 
cause  of  diffuse  abdominal    pain,  especially  in  poorly-nourished 
women  with  lax  abdominal  walls.     Here  again,  local  examination, 
of  the  abdomen  will  reveal  the  cause. 

Before    leaving    the    subject    of    abdominal    pains,    we    must 

1  Brain,  1901,  vol.  xxv.  p.  373. 


192  NERVOUS    DISEASES 

not  fail  to  recall  the  familiar  crises  of  tabes  dorsalis  : — gastric 
crises  associated  with  pain  and  vomiting,  intestinal  crises  associated 
with  colic  and  diarrhoea,  diaphragmatic  crises  with  hiccough, 
bladder  crises,  &c.  All  these  may  closely  simulate  the  pain  of 
acute  abdominal  disease.  But  the  history  of  the  case,  together 
with  an  investigation  of  the  pupils,  knee-  and  ankle -jerks,  and 
the  other  phenomena  of  tabes,  will  usually  save  us  from  error. 

Lumbago,  or  pain  in  the  lumbar  muscles,  a  variety  of 
myalgia,  is  usually  easily  recognised.  The  pain  is  intensified 
by  active  muscular  contraction  and  also  by  passive  stretching, 
caused  for  instance  by  the  stooping  posture.  It  is  also  associated 
with  tenderness  on  pressure.  Lumbo -abdominal  neuralgia,  on 
the  other  hand,  is  a  diffuse  and  more  superficial  pain,  not  confined 
to  the  lumbar  region  but  spreading  forwards  to  the  front  of 
the  abdomen,  and  sometimes  to  the  groin,  genitals  or  gluteal 
region.  It  is  paroxysmal,  and  during  the  paroxysm  there  may 
be  cramp-like  spasms  of  the  abdominal  muscles  or  of  the  cremaster. 
It  is  associated  with  the  "  tender  points  "  of  a  true  neuralgia, 
these  being  situated  over  the  vertebral  spines,  the  iliac  crests,  the 
linea  alba,  inguinal  canal,  scrotum  or  labium.  Sacral  pain  is  often 
due  to  uterine  disease,  as  in  the  famihar  uterine  dysmenorrhoea 
or  the  well-known  pains  of  labour. 

Coccygodynia,  or  neuralgic  pain  in  the  region  of  the  coccyx,  is 
commoner  in  female  patients  than  in  males.  The  pain  is  rarely 
continuous.  More  usually  it  is  induced  by  sitting  or  walking,  or 
by  the  contraction  of  any  of  the  muscles  attached  to  the  coccyx, 
e.g.  during  defsecation.  It  is  often  associated  with  local  tender- 
ness, especially  on  rectal  examination.  The  pain  is  located  not 
only  in  the  coccyx  but  also  in  the  soft  parts  just  distal  to  the  tip 
of  the  bone.  Its  usual  cause  is  a  dislocation  or  fracture-disloca- 
tion of  the  coccyx,  either  from  a  fall  or  kick  upon  the  coccyx,  or 
as  a  result  of  an  internal  trauma,  especially  prolonged  labour. 
It  may  also  occur  as  a  symptom  of  tabes  dorsahs  and  is  not  un- 
cc>mmon  in  hysteria,  particularly  in  traumatic  hysteria. 

Pains  in  the  Limbs. — Brachial  neuralgia,  generally  a  uni- 
lateral affection,  is  referred,  as  a  rule,  to  the  whole  area  of  distribu- 
tion of  the  plexus,  namely  to  the  lower  part  of  the  neck,  the 
shoulder  and  the  whole  upper  limb,  being  most  intense  in  the 
proximal  part  of  the  limb.  It  is  rare  to  meet  with  neuralgia 
confined  to  an  individual  nerve-area,  such  as  that  of  the  median 


PAIN  193 

or  ulnar,  except  in  cases  of  local  injury  or  disease  of  the  nerve- 
trunks.  The  pain  of  brachial  neuralgia  is  aggravated  by  move- 
ment of  the  limb,  which  feels  heavy  and  numb,  though  there  is  no 
paralysis.  The  "  tender  points  "  are  over  the  nerve-trunks,  such 
as  the  musculo-spiral,  circumflex,  median  or  ulnar  nerves. 

If  anaesthesia  or  trophic  changes  be  superadded,  Ave  probably 
have  to  do  with  structural  changes  in  the  nerve-trunk,  that  is, 
with  a  neuritis,  not  a  mere  neuralgia.  In  every  case  of  brachial 
neuralgia  we  must  carefully  examine  the  nerve-trunks  in  their 
entire  course,  to  exclude  the  possibility  of  organic  lesions  com- 
pressing or  infiltrating  the  nerves.  In  addition  to  pain,  brachial 
neuritis  often  produces  weakness  and  atrophy  of  the  corre- 
sponding muscles,  and  impairment  or  perversion  of  cutaneous 
sensation. 

Analogous  to  brachial  neuralgia  and  neuritis  in  the  upper  limb, 
we  have  in  the  lower  limb  sciatica,  a  te:m  which  includes  sciatic 
neuralgia  and  sciatic  neuritis.  In  every  case  of  so-  called  sciatica 
we  have  to  decide  which  of  these  two  is  present.  Many  cases  of 
sciatic  neuralgia  occur  independently  of  any  affection  of  the  sciatic 
nerve,  e.g.  in  vertebral  disease,  tuberculous  or  anthritic,  in  affections 
of  the  sacro-iliac  joint  or  of  the  hip-joint,  in  diseases  of  the 
femur  (tumours,  osteomyelitis,  &c.),  in  intermittent  arterial  clau- 
dication, &c.  In  true  sciatic  neuralgia  there  is  usually  a  dull, 
aching  pain,  more  or  less  constant,  in  the  back  of  the  thigh,  with 
occasional  paroxysms  of  darting  or  boring  pain,  generally  from 
above  downwards,  along  the  course  of  the  sciatic  nerve.  Any 
movement  of  the  limb  whereby  the  nerve  is  made  tense,  or  any 
local  pressure  as  from  sitting  on  a  hard  chair,  brings  on  a  paroxysm. 
Therefore  the  patient  habitually  keeps  the  hip  and  knee  sHghtly 
flexed  on  the  affected  side,  so  as  to  relax  the  nerve.  It  is  not 
uncommon  to  find  a  slight  scoliosis  in  the  lumbar  region,  the  con- 
cavity being  towards  the  sound  side.  The  "  tender  points  "  are 
at  the  fifth  lumbar  spine  (especially  on  lateral  pressure  from  the 
affected  towards  the  healthy  side  ^)  over  the  posterior  iliac  spine, 
the  sciatic  notch,  the  popliteal  space,  the  peroneal  nerve  below 
the  head  of  the  fibula,  and  behind  the  malleoli.  Some  cases  of 
sciatica  are  associated  with  marked  tenderness  on  deep  pressure 
through  the  abdominal  wall  towards  the  vertebral  column,  at  a 
level  one  finger' s-breadth   below  the  umbilicus  and  two  fingers'- 

1  Kaimist,  Neurolog.  Centralbl.,  1C09,  p.  1087. 

N 


194  NERVOUS    DISEASES 

breadth  laterally  from  that  point,  on  the  side  of  the  sciatic  pain  ; 
pressure  on  the  corresponding  spot  on  the  healthy  side  being  pain- 
less.^ Passive  stretching  of  the  nerve  increases  the  pain,  for 
example  by  flexion  of  the  hip  with  the  knee  extended.  Blunting 
of  sensation  in  the  peroneal  or  posterior  tibial  area  is  uncommon 
and  indicates  an  organic  neuritis  or  perineuritis,  as  also  do  any 
alterations  in  the  electrical  reactions  of  the  muscles,  or  any  con- 
siderable degree  of  muscular  atrophy.  In  sciatic  neuritis  the 
temperature  of  the  limb  is  generally  lower  than  on  the  healthy 
side.  The  ankle-jerks  should  always  be  tested  on  both  sides.  In 
sciatic  neuritis  the  jerk  may  be  diminished  or  lost,  whereas  in 
neuralgia  it  remains  normal.  In  both  affections  we  may  observe 
exaggeration  of  the  cremasteric  reflex  on  the  affected  side.  The 
reflex  of  the  tensor  fasciae  femoris,  which  in  neuritis  of  the  sciatic 
trunk  is  unaffected,  is  usually  lost  when  the  neuritis  implicates  the 
lumbo-sacral  roots  from  which  the  sciatic  arises.^ 

Varicose  (or  phlehogenic)  sciatica  ^  is  a  variety  of  sciatic  neuralgia 
in  which  the  small  veins  within  the  sciatic  trunk  have  become 
dilated  and  varicose.  The  symptoms  are  characteristic.  The 
patient  has  inveterate  pains  in  the  sciatic  region,  often  accompanied 
by  painful  reflex  cramps  of  the  gluteal  muscles.  The  sciatic  pain 
is  induced  by  slow  walking  or  by  standing  about,  whereas  brisk 
walking,  or  more  violent  exertion,  e.g.  hill- climbing,  cycling,  &c., 
relieves  the  pain.  The  pain  also  disappears  on  lying  down.  If 
the  patient  be  examined  in  the  recumbent  posture,  no  abnormality 
may  be  detected,  but  if  he  is  examined  standing  up,  we  sometimes 
observe  at  the  site  of  maximum  pain,  e.g.  in  the  popliteal  space  or 
below  the  head  of  the  fibula,  a  slight  puffiness  or  swelling.  Occa- 
sionally there  is  also  well-marked  varicosity  in  the  larger  sub- 
cutaneous veins.  It  is  important  to  recognise  this  variety  of  sciatica 
since  ordinary  drugs  and  counter-irritants  fail  to  alleviate  it — 
whereas  gentle  elastic  pressure  often  relieves  it  at  once. 

Meralgia  paresthetica  is  a  variety  of  neuralgia  occurring  in  the 
area  of  distribution  of  the  external  cutaneous  nerve  of  the  thigh. 
It  consists  in  parsesthesia  or  actual  pain  in  the  outer  aspect  of  one 
thigh.  The  pain  is  often  induced  by  standing  or  walking,  possibly 
owing  to  stretching  of  the  fascia  lata.  In  some  cases  it  results 
from  the  pressure  on  the  nerve  by  a  badly-fitting  corset.     It  is 

1  Gara,  Deutsche  med.  Wcchenschrift,  1911,  No,  16. 

2  Bonola,  Revue  neurologique,  Sept.  1912,  p.  324. 
^  Edinger,  Berlin  klin.  Wochensch.,  1914,  No.  U. 


PAIN  195 

sometimes  associated  with  flat-foot  on  the  same  side.  Here,  as 
in  brachial  or  sciatic  pain,  the  presence  of  an  area  of  impaired 
sensation  would  indicate  a  neuritis  rather  than  a  neuralgia. 

In  rarer  cases  we  may  find  neuralgia  in  the  area  of  the  anterior 
crural  or  of  the  obturator  nerve,  and  this  may  be  symptomatic  of 
an  intra-pelvic  tumour,  or  of  an  obturator  hernia. 

The  pains  of  brachial  or  sciatic  neuralgia  and  neuritis,  and  of 
meralgia  parsesthetica,  are  unilateral.  Let  us  now  consider  the 
bilateral  pains  which  may  be  met  with  in  the  limbs. 

Bilateral  pains  should  always  suggest  to  our  minds  either  a  toxic 
cause  attacking  the  peripheral  nervous  structures  of  both  Hmbs,  or 
some  central  disease  of  the  spinal  meninges  affecting  the  posterior 
roots  bilaterally,  or  again  some  angio-neurotic  condition  such  as  Ray- 
naud's disease,  erythromelalgia,  or  intermittent  arterial  claudication 

Pains  in  the  muscles  or  joints  are  a  common  symptom  in  people 
who  work  under  compressed  air,  as  in  divers  or  workers  in  deeply 
sunk  caissons,  whether  under  ground  or  under  water.  The 
symptoms  of  caisson  disease,  or  "  decompression  paraplegia,"  are 
most  likely  to  occur  when  the  worker  ascends  too  abruptly  to  the 
ordinary  atmosphere.  All  such  workers  ought  to  pass  through 
a  "  decompression-chamber,"  where  the  atmospheric  pressure  is 
gradually  reduced  to  normal.  If  this  be  not  done,  bubbles  of 
nitrogen  are  set  free  in  the  blood  and  may  either  form  emboli 
in  the  arterioles  of  the  central  nervous  system  with  consequent 
small  foci  of  necrosis,  or  the  nitrogen  may  effervesce  or  explode  out 
of  the  capillaries  into  the  nervous  tissues,  especially  into  the  sub- 
stance of  the  spinal  cord.  Capillary  haemorrhages  may  also  occur. 
Clinically  in  such  cases  not  only  have  we  severe  pains  in  the  limbs 
but  also  aural  symptoms  due  to  labyrinthine  affection  : — deafness, 
giddiness  and  tinnitus,  sometimes  even  actual  rupture  of  the 
tympanic  membrane.  There  may  also  be  anaesthesia  and  para- 
plegia of  spinal  type,  and  such  paralysis  may  be  permanent. 
Slighter  cases  clear  up  quickly,  if  the  air-extravasation  has  been 
merely  from  the  capillaries  without  air-embolism  of  the  arterioles. 

The  lightning  pains  of  tabes  may  be  unilateral  or  bilateral. 
They  are  commoner  in  the  legs  than  in  the  arms,  since  tabes  is  a 
disease  which  generally  begins  in  the  posterior  root-fibres  of  the 
lumbo-sacral  region.  These  pains  are  variously  described  by  the 
patient  as  stabbing,  burning,  tearing,  or  bursting,  and  are  commonly 
associated  with  local  hypersesthesia  of  the  skin.    They  are  frequently 


196  NERVOUS    DISEASES 

mistaken  for  rheumatic  pains,  and  all  the  more  so  inasmuch  as 
they  often  coincide  with  changes  in  the  weather. 

Tight  "  tourniquet  "  pains  around  the  lower  limbs,  in  broad 
zones  rather  than  narrow,  are  sometimes  an  early  and  persistent 
symptom  in  disease  of  the  lumbo-sacral  region  of  the  cord.  They 
are  due  to  irritation  of  the  posterior  roots,  and  may  also  occur  in 
tabes.  Root-pains  also  occur,  though  less  commonly,  in  certain 
cases  of  multiple  sclerosis. 

The  root-pains  of  tumour  or  inflammation  of  the  spinal  men- 
inges, or  of  spinal  caries  or  tumour,  are  more  or  less  constant, 
with  paroxysmal  exacerbations.  Inflammatory  affections  of  the 
meninges  are  usually  bilateral  from  the  outset,  with  corresponding 
bilateral  pains.  But  in  cases  of  meningeal  tumour  the  pains  are 
generally  unilateral  at  first,  and  become  bilateral  as  the  disease 
spreads  to  the  opposite  side.  The  level  of  the  pains  in  meningeal 
disease  varies  with  the  level  of  the  affected  posterior  roots.  Thus 
in  cervical  meningitis,  tumour  or  caries,  there  is  pain  in  the  neck, 
spreading  down  one  or  both  arms  along  the  corresponding  root- 
areas  ;  in  thoracic  cases  the  pain  is  around  the  trunk,  and  in 
lumbar  or  sacral  cases  it  is  in  various  parts  of  the  lower  limbs. 
The  recto-perineal  pain  of  certain  cauda  equina  lesions  is  pecuHar 
in  that  it  occurs  in  the  sitting  posture  only,  and  disappears  when 
the  patient  lies  down  or  stands  up,  so  as  to  relax  the  adherent 
sacral  roots.  Meningeal  pain  is  often  associated  with  local  hyper- 
sesthesia  corresponding  to  the  uppermost  roots  affected,  and  with 
tonic  spasms  of  the  muscles  at  that  level.  If  the  meningeal  lesion 
affects  the  cord  within,  whether  by  compression  or  by  infiltration, 
there  will  be  in  addition  to  root-pains  the  other  signs  of  organic 
cord  disease — so-called  'paraplegia  dolorosa,  with  its  anaesthesia, 
motor  weakness  and  alterations  of  reflexes  below  the  level  of  the 
lesion.  Inflammatory,  tuberculous  and  syphilitic  affections  of  the 
spinal  meninges  are  always  associated  with  cellular  changes  in  the 
cerebro- spinal  fluid  (see  p.  439). 

Affections  of  the  peripheral  nerves  may  also  produce  pain. 
Thus  in  peripheral  neuritis  there  is  not  only  pain,  with  hypersesthesia 
of  the  skin  of  the  feet  and  hands,  but  there  is  intense  muscular 
tenderness  on  pressure,  together  with  a  degree  of  tactile  anaesthesia, 
and  in  severe  cases  muscular  paralysis  and  muscular  atrophy, 
accompanied  by  the  reactions  of  degeneration. 

Pains  localised  in  single  nerve-areas  should  always  lead  us  to 


PAIN  197 

examine  the  nerve-trunk  in  its  entire  extent.  Tubercula  dolorosa 
are  multiple  growths  (usually  neuro-fibromata)  in  the  connective 
tissue  of  the  nerve-trunks,  many  of  them  forming  little  subcutaneous 
nodules  easily  palpable  and  exquisitely  tender,  others  less  acces- 
sible in  the  deeper  nerve-trunks,  causing  referred  pains  in  the 
particular  nerve  areas.  If  these  growths  not  merely  irritate  but 
interrupt  the  nerve-fibres  within  the  nerve-trunks,  there  may, 
in  rare  cases,  be  areas  of  anaesthesia.  Clinically  we  seldom  find 
motor  paralysis  from  such  growths,  except  as  a  result  of  pressure 
on  the  spinal  cord  or  base  of  the  brain  by  a  neuroma  on  one  of  the 
spinal  or  cranial  nerve-roots. 

It  is  convenient  here  to  refer  to  erjdihromelalgia,  characterised  by 
cyanosis  and  pain  in  one  or  both  feet  in  the  dependent  posture, 
relieved  by  elevating  the  limb  ;  to  Raynaud's  disease,  which  may  be 
associated  not  only  with  local  pallor,  cyanosis  or  gangrene,  but  also 
with  subjective  sensations  of  tinghng  or  pain  ;  and  to  intermittent 
arterial  claudication,  in  which  the  patient  after  a  few  steps  becomes 
unable  to  walk  farther,  owing  to  intolerable  pain  in  the  muscles 
of  the  leg.  To  these  conditions  we  shall  return  later,  when  study- 
ing the  nervous  affections  of  the  vascular  system. 

Paroxysmal  spontaneous  pain  in  the  periphery  of  a  limb, 
ascending  towards  the  trunk,  sometimes  occurs  as  a  variety  of  sen- 
sory fit  in  gross  disease  of  the  cortical  sensory  areas  in  the  contra- 
lateral post-central  gyrus.  Thus  in  one  case  of  my  own,  in  which 
there  was  a  focal  lesion  of  the  left  post -central  gyrus,  the  earliest 
symptom  was  paroxysmal  pain  in  the  right  fingers  and  hand.^ 

Finally,  we  should  refer  to  the  group  of  pains  met  with  in 
hysteria  and  neurasthenia.  These  are  more  often  areas  of  hyper- 
sesthesia  than  of  spontaneous  pain.  They  are  specially  common 
in  the  neighbourhood  of  joints,  whose  slightest  movement  causes 
intense  pain.  In  other  cases  the  muscles  are  apparently  hyper- 
sensitive, so  that  any  attempt  at  movement  of  the  limb,  active 
or  passive,  causes  an  illusion  of  pain — so-called  akinesia  algera, 
of  psychical  origin.  But  the  history  of  the  case,  in  which  there 
has  often  been  a  preceding  local  injury,  the  absence  of  signs  of 
structural  disease,  local  or  central,  and  the  presence  of  other 
hysterical  or  neurasthenic  phenomena,  will  aid  us  in  our  diagnosis. 
It  may  be  necessary  to  give  a  general  anaesthetic  in  order  to 
eliminate  gross  local  organic  disease. 

^  Review  of  Neurol,  and  PsycJiiatry,  1908,  p.  379. 


CHAPTEH  XII 

ABNORMALITIES   OF   SENSATION: 
HYPERiESTHESIA,   PARESTHESIA,   ANESTHESIA 

We  have  already  considered  tlie  anatomical  course  of  the  chief 
sensory  paths  from  the  periphery  to  the  perceiving  centres  in  the 
brain  (Chapter  I.).  Let  us  now  proceed  to  consider  the  methods 
of  clinical  investigation  of  the  various  forms  of  sensation. 

All  parts  of  the  surface  of  the  body  are  not  equally  sensitive. 
Thus  the  tip  of  the  tongue,  the  lips,  the  iinger-tips,  in  the  order 
mentioned,  are  most  sensitive  to  surface  impression,  whilst 
other  parts  such  as  the  dorsal  aspect  of  the  trunk,  the  upper  arm, 
and  the  calf  of  the  leg,  are  least  sensitive.  These  differences  de- 
pend on  various  factors,  such  as  thickness  of  epithelium,  relative 
abundance  of  sensory  end-organs,  &c.,  into  which  we  need  not 
enter  more  minutely  here. 

All  sorts  of  ingenious  apparatus  have  been  devised  for  the 
accurate  measurement  of  minute  differences  in  sensibility  to  touch, 
pressure,  pain,  temperature,  and  so  on.  But  for  clinical  purposes, 
we  should  avoid  complicated  apparatus  and  content  ourselves 
with  the  simplest  possible  methods  which,  whilst  accurate  enough 
for  practical  purposes,  do  not  impose  too  great  a  strain  on  the 
patient's  attention  nor  demand  too  high  a  degree  of  intelligence 
on  his  part. 

The  most  important  varieties  of  sensory  stimuli  which  we 
employ  in  testing  a  patient's  sensory  functions  are  hght  touches, 
pin-pricks,  cold  and  hot  objects,  all  of  which  refer  to  cutaneous 
sensations.  We  have  also  to  consider  other  sensations  from  deeper 
structures,  such  as  joint-sensation  (or  sense  of  position  on  passive 
movement),  active  muscle-sensation  (kineesthetic  sense,  or  sense  of 
active  muscular  contraction),  and,  lastly,  the  vibration  sensation 
produced  when  a  sounding  tuning-fork  is  placed  over  the  sub- 
cutaneous surface  of  a  bone  or  upon  a  finger-nail.  There  are  other 
varieties  of  sensory  stimuh,  such  as  electro-cutaneous  sensibility 
(which  is  generally,  but  not  always,  parallel  in  intensity  with  the 

198 


ABNORMALITIES   OF    SENSATION  199 

pain-sense),  and  there  is  the  sensation  of  pressure  and  appreciation 
of  differences  of  pressure,  &c.  But  these,  though  physiologically- 
interesting,  ar-  of  minor  clinical  value. 

There  is  perhaps  no  better  criterion  of  neurological  dexterity 
than  the  accuracy  with  which  an  observer  can  map  out  areas  of 
diminution  or  loss  of  sensation  on  the  one  hand,  or  of  perverted 
or  exalted  sensation  on  the  other.  Both  experience  and  patience 
are  required,  in  order  to  obtain  trustworthy  results. 

Inasmuch  as  we  are  largely  dependent  on  the  intelligence  and 
goodwill  of  our  patient  for  accurate  answers,  we  must  try,  as  far 
as  possible,  to  eliminate  all  distracting  outside  factors.  Therefore 
we  direct  the  patient  to  close  his  eyes  when  we  are  testing 
sensation,  so  that  his  attention  may  not  be  diverted  by 
watching  what  is  being  done.  We  must  also  be  careful  not 
to  weary  a  patient  by  too  prolonged  examination,  lest  as 
he  gets  tired  or  impatient  his  answers  become  inaccurate.  The 
simpler  our  methods  of  examination,  the  better  are  our  results 
likely  to  be.  We  have  also  to  contend  with  wide  variations  in 
the  intelHgence  of  different  patients,  in  their  education,  and  in 
their  attentiveness ;  this  latter  may  be  modified  by  pain,  by 
anxiety,  or  by  psychical  deficiencies.  Sometimes  we  have  to 
deal  with  deliberate  attempts  on  the  part  of  the  patient  to  mislead 
us.  Fortunately,  patients  who  simulate  disease  generally  make 
blunders  so  gross  as  to  prevent  an  erroneous  diagnosis  on  the 
part  of  a  careful  observer.  Of  course  the  physician  must  be  care- 
ful to  avoid  suggesting  the  presence  of  sensory  changes  to  the 
patient  under  examination. 

Clinical  Investigation  of  Sensation. — At  the  start,  the 
patient's  eyes  should  be  closed,  or  some  object  should  be  inter- 
posed between  his  eyes  and  that  part  of  the  body  which  is  being 
tested.  We  then  proceed  to  test  the  various  cutaneous  sensations — 
touch,  pain  and  temperature,  separately  and  in  turn. 

Touch  is  tested  by  means  of  some  soft  light  object,  such  as  a 
tuft  of  cotton-wool,  a  feather,  or  by  gentle  pulling  or  stroking  of 
the  hairs.  The  compass  test  of  epicritic  sensibiHty  is  carried  out 
by  placing  the  points  of  a  pair  of  blunt  compasses  on  the  skin  and 
observing  at  what  degree  of  separation  the  patient  can  recognise 
two  points  instead  of  one.  Loss  of  sensation  in  the  hairs  is  called 
"  tricho-ansesthesia."  Pressure  is  tested  by  means  of  a  pencil  or 
other  blunt  object ;  if  such  pressure  be  steadily  increased  a  "  deep  " 


200  NEKVOUS   DISEASES 

sensation  of  pain  is  ultimately  produced.  Cutaneous  pain  is 
tested  by  pricking,  or  better  by  scratching,  with  a  sharp  needle  ; 
itching  by  rubbing  in  the  hairs  of  mucuna  pruriens  ;  cold  by  blow- 
ing on  the  skin,  or  by  a  cold  object  such  as  a  metal  spoon  or  a 
test-tube  containing  ice-cold  water  ;  heat  by  breathing  on  the  skin 
or  by  a  warm  object  such  as  a  test-tube  containing  hot  water,  or 
a  metal  spoon  which  has  just  been  removed  from  a  jug  of  hot  water 
at  about  50°  C.  Higher  temperatures  produce  sensations  of  pain 
rather  than  of  heat  alone. 

Each  variety  of  sensation  should  be  examined  separately,  before 
passing  on  to  the  next  kind  of  stimulus,  and  the  results  should  be 
recorded  on  an  outline-chart  of  the  body.  In  mapping  out  areas 
of  abnormal  sensation,  it  is  useful  to  have  a  skin-pencil  with  which 
to  mark  the  patient's  skin,  before  copying  the  result  on  our  chart. 
An  important  practical  point  in  mapping  out  areas  of  anaesthesia, 
is  to  begin  within  the  ansesthetic  area,  and  to  work  towards  the 
normal  skin,  not  in  the  reverse  direction.  It  is  easier  for  a  patient 
to  recognise  the  moment  when  he  first  feels  a  sensation  than  for 
him  to  observe  when  he  first  loses  it.  On  the  other  hand,  in 
mapping  out  areas  of  hypersesthesia  or  of  parsesthesia,  we  should 
work  from  normal  skin  towards  the  hypersesthetic  area,  asking 
the  patient  to  call  out  as  soon  as  his  sensation  changes. 

In  setting  about  the  examination  of  the  sensory  functions,  we 
usually  begin  with  that  of  touch.  The  patient's  eyes  being  closed, 
we  touch  him  lightly  on  both  sides  of  the  face  simultaneously 
and  observe  not  only  whether  he  feels  the  touches,  but  whether 
they  are  equally  distinct  on  the  two  sides.  We  then  touch  sym- 
metrical spots  on  the  neck,  shoulders,  hands,  trunk,  and  lower  limbs. 
We  next  proceed  to  do  the  same  with  light  needle-scratches,  then 
with  cold  and  with  warm  objects.  If  the  patient  has  an  area  of 
diminished  or  altered  sensibility,  we  generally  discover  it  by  this 
method.  When  we  find  an  area  of  abnormality,  we  proceed  to  map 
it  out  carefully,  making  separate  observations  for  touch,  pain,  and 
temperature,  and  noting  whether  the  areas  coincide  or  overlap. 

Besides  noting  whether  a  patient  feels  a  stimulus,  for  instance  a 
tactile  one,  we  should  also  notice  whether  he  localises  it  accurately. 
This  is  accomplished  by  asking  him  to  place  his  finger  on  the  spot 
where  he  was  touched,  for  instance,  the  dorsum  of  the  hand.  A 
normal  individual  can  do  this  accurately  to  within  a  fraction  of  an 
inch.     But  in  certain  varieties  of  anaesthesia,  especially  in  cortical 


ABNORMALITIES    OF    SENSATION  201 

lesions,  the  patient,  whilst  able  to  tell  that  he  has  been  touched, 
makes  an  error  of  several  inches  in  locahsation.  This  is  called 
"  atopognosis."  Horsley  ^  maintains  that  errors  in  the  localisa- 
tion of  cutaneous  impressions  are,  in  cases  of  cortical  lesions,  always 
in  a  proximal  direction,  i.e.  the  patient  refers  the  stimulus  to  a 
point  higher  up  the  limb,  but  Head  and  Holmes ''  find  no  such 
constancy  if  the  test  is  carried  out  by  making  the  patient  indicate 
the  corresponding  spot  on  the  hand  of  a  bystander.  Sometimes 
the  patient,  when  touched  on  one  side  of  the  body,  feels  the  sensa- 
tion at  the  corresponding  spot  on  the  opposite  side.  This  is 
termed  "  allocheiria,"  and  occurs  in  certain  cases  of  hysteria. 

When  testing  pain,  we  sometimes  find  that  although  the  patient 
correctly  perceives  and  localises  the  stimulus,  there  is  an  abnormally 
long  interval  of  time,  perhaps  amounting  to  several  seconds,  be- 
tween the  stimulus  and  the  patient's  perception  of  pain.  This  is 
called  "  delayed  sensation,"  and  is  met  with  chiefly  in  cases  of  tabes. 

The  path  for  itching  sensation  appears  to  run  along  with  the 
pain-fibres.  Thus  in  organic  lesions  producing  analgesia  (e.g. 
syringomyelia,  &c.)  the  normal  sensation  of  itching  produced  by 
the  application  of  mucuna  pruriens  to  the  skin  is  lost  in  the  anal- 
gesic area.^  In  areas  of  hypalgesia  pin-pricks  may  cause  itching 
instead  of  pain,  whilst  ynucuna  pruriens  induces  a  subnormal  degree 
of  itching. 

When  charting  areas  of  very  slight  cutaneous  anaesthesia,  it  is 
often  difficult,  despite  the  utmost  care  as  regards  our  stimuli,  to 
obtain  an  exact  outline  of  the  area  of  altered  sensibility.  Changes 
in  the  quality  of  sensations  may  exist  which  are  undetectable 
even  by  cotton-wool  touches.  Nevertheless  the  patient,  if  he 
tests  his  own  skin,  may  be  conscious  of  an  abnormality  too  delicate 
to  be  discovered  by  another  person  on  objective  examination. 
But  if  we  have  a  specially  intelligent  patient  and  get  him  to  explore 
his  ansesthetic  area  by  stroking  with  his  own  finger,  indicating 
where  he  perceives  a  line  of  transition  between  normal  and  abnormal, 
it  is  often  possible  for  him,  by  such  "  auto -exploration,"  to  map 
out  the  area  of  altered  sensibility  with  great  accuracy.^ 

If  a  fold  of  skin  be  lifted  up  between  the  finger  and  thumb 
and  pulled  in  various  directions,  upwards,  downwards,  or  sideways, 
a  normal  person  can  always  recognise  the  direction  in  which  his 

1  Brain,  1906,  p.  137.  ^  md,^  1911,  pp.  161-164. 

^  Thole,  Neurologisches  Centralhlatt,  1912,  s.  GIO. 

*  Trotter  and  Davies,  Rev.  of  Neurol,  and  Psych.,  1907,  p.  701. 


202  NERVOUS  -DISEASES 

skin  is  being  displaced. ^  Sometimes,  however,  in  early  tabes  the 
direction  of  traction  of  the  skin  and  subcutaneous  tissue  is  lost 
over  a  wide  area,  and  this  phenomenon  may  be  present  long  before 
any  cutaneous  tactile  anaesthesia  or  analgesia  can  be  made  out. 

So  much  for  cutaneous  and  subcutaneous  sensations.  But 
there  are  other  forms  of  sensation  which  are  of  clinical  import- 
ance. Joint-sense  is  tested  by  moving  a  joint  passively  into  various 
positions  backwards  and  forwards,  then  holding  it  fixed  in  a  cer- 
tain position,  such  as  that  of  semi-fiexion,  and  asking  the  patient 
to  imitate  exactly  that  position  with  the  limb  of  the  opposite  side. 
During  this  test  the  muscles  of  the  joint  under  examination  must 
be  fully  relaxed,  for  it  not  infrequently  happens  that  when  a 
patient  is  in  doubt  as  to  the  position  of  his  joint,  he  begins  to  make 
slight  voluntary  movements  of  the  joint  before  answering.  These 
must  not  be  permitted,  since  he  thereby  gains  information  as  to 
the  position  of  the  limb,  not  from  his  joint-sense  but  through  an 
entirely  different  sense,  viz.  the  kineesthetic  sense  or  sense  of  active 
muscular  contraction. 

To  test  this  hincesthetic  sense,  we  notice  whether  the  patient,  when 
raising  his  limbs,  can  detect  di:fferences  in  the  weights  of  objects 
of  similar  size,  for  example  a  shilhng  and  a  sovereign,  either 
placed  in  his  hand,  or  hung  in  a  sling  over  his  hand  or  foot.  For 
this  purpose  we  sometimes  employ  a  series  of  leather  or  wooden 
balls  of  equal  size,  loaded  with  difierent  weights.  Normally, 
according  to  Weber's  law,  a  healthy  individual  should  detect  an 
increase  of  one-third  in  the  weights  of  two  successive  objects. 
Tabes  is  the  disease  in  which  this  sense  of  active  muscular  con- 
traction is  most  markedly  diminished,  and  in  which  the  joint-sense 
is  notably  impaired  also.  The  loss  of  these  two  senses  is  probably 
the  main  factor  in  the  production  of  tabetic  ataxy.  Loss  of 
kinsesthetic  sense  is  also  present  in  many  cases  of  "  cortical " 
ansesthesia. 

^,We  purposely  avoid  using  the  term  "  muscular  sense,"  for 
several  reasons.  Firstly,  it  is  ambiguous,  since  it  has  been  used  to 
include  two  entirely  different  senses  : — joint-sense  and  kinaesthetic 
sense.  Moreover,  it  might  also  be  confounded  with  a  third  sense, 
the  sensibility  of  muscles  to  deep  pressure  with  the  fingers.  Normally 
such  pressure,  if  moderate  in  degree,  is  painless  ;  but  in  certain 
diseases,  as  in  peripheral  neuritis,  in  the  various  forms  of  myositis, 

1  Bayer,  Munch,  med.  Wochensch.,  May  1914,  p.  1105. 


ABNORMALITIES    OF    SENSATION 


203 


and  in  the  abdominal  muscles  superficial  to  an  area  of  peritonitis, 
the  muscles  become  exquisitely  tender  to  the  lightest  pressure. 
On  the  other  hand,  it  is  common  to  find  in  tabes  that  severe  com- 
pression of  the  muscles  and  tendons,  for  example  of  the  leg 
muscles,  and  especially  of  the  tendo  Achillis,  is  painless  (Abadie's 
sign).  This  muscle  and  tendon  analgesia  is  often  present  in 
early  stages  of  the  disease. 

It  is  sometimes  of  value  to  observe  the  patient's  power  of 
recognising,  without  seeing  them,  the  forms  of  soHd  objects  placed 
in  his  hand — so-called  stereognostic  perception.  Normally  a  patient 
should  be  able  to  recognise  familiar  objects 
such  as  a  key,  a  coin,  or  a  chain.  But  in 
some  cases  the  patient,  though  able  to  feel 
the  presence  of  some  object,  cannot  describe 
its  form  and  qualities,  without  seeing  it. 
Such  "  astereognosis "  is  due  to  impair- 
ment of  sensation,  whether  from  peripheral 
disease,  from  thalamic  lesions,  or  from  disease 
in  the  cortical  centres. 

Lastly,  there  is  the  vibration-sense  (pallses- 
thesia,  or  "  osseous  sense  ")  described  origin- 
ally by  Egger.     This  is  tested  by  means  of  Fi«.  86 -Tabes  with  loss 

./       ./        oo  ^  "^ .  .  of  vibration-sense    in 

a  low-pitched  tumng-iork,  which  is  set  into 
vibration  and  placed  upon  the  subcutaneous 
surface  of  a  bone.  In  normal  individuals 
a  characteristic  vibratile  thrill  is  felt.  But 
in  certain  diseases  involving  the  posterior 
roots,  such  as  tabes,  or  in  transverse  lesions  of  the  spinal  cord, 
the  vibration-sense  may  be  lost  in  the  bones  corresponding  to 
the  affected  roots  (Fig.  86).  Loss  of  this  sense  may  be  the 
earliest  form  of  anaesthesia  in  root-lesions  as  in  tabes,  where  it 
sometimes  precedes  cutaneous  anaesthesia.  In  Brown-Sequard 
paralysis  vibration-sense  is  lost  on  the  same  side  as  the  muscular 
paralysis^  (see  Figs.  11  and  14).  But  the  vibration-sense  is  not 
an  exclusive  property  of  bones,  though  bones  are  most  strikingly 
sensitive  ;  it  can  be  perceived  in  other  tissues,  notably  in  the 
nails,  which  are  closely  connected  with  the  periosteum,  and  even 
in  the  connective-tissues,  although  in  them  less  intensely. 

Excessive  sensitiveness  to  normal  stimuU  is  termed  Tiyperces- 

^    Vide  Bing,  Neurolog.  Centralblatt,  1910,  p.  173. 


bones  of  lower  limbs, 
pelvis,  lumbar,  and 
lower  dorsal  vertebrae. 
The  bones  with  loss 
of  vibration-sense  are 
shaded  black. 


204  NERVOUS    DISEASES 

thesia.  Such  hypersesthesia  is  usually  accompanied  by  a  degree 
of  discomfort  or  even  pain,  even  though  a  stimulus  be  used  which 
is  ordinarily  painless.  The  term  farcesthesia,  or  perversion  of 
sensation,  signifies  that  an  ordinary  stimulus  evokes  an  unusual 
sensation,  as  for  example  a  feeling  of  tingling  when  the  skin  is 
touched,  or  a  feeling  of  acute  pain  when  moderate  cold  is  applied. 
Under  the  head  of  parsesthesiae  we  may  also  include  such  pheno- 
mena as  multiple  sensations  (polysesthesia),  allocheiria,  &c. 

Strictly  speaking,  diminution  of  sensation  should  be  designated 
hypo-CBsthesia,  and  the  term  anaesthesia  should  be  reserved  for  total 
loss  of  sensation.  It  is  usual,  however,  to  speak  of  "  slight," 
"  moderate,"  and  "  total "  anaesthesia.  When  only  one  form  of 
cutaneous  anaesthesia  is  referred  to,  we  sometimes  find  it  con- 
venient to  talk  of  tactile  ancesthesia,  of  analgesia  or  loss  of  pain- 
sense,  and  of  thermo-ancesthesia  or  loss  of  temperature -sense. 
We  speak  of  dissociated  ancesthesia  when  some  forms  of  sensation, 
such  as  tactile  sense,  are  normal,  whilst  in  the  same  area  others, 
such  as  pain  and  temperature -sense,  are  lost.  This  occurs  especially 
in  syringomyeha  and  in  the  Brown-Sequard  syndrome. 

We  speak  of  hemi- ancesthesia  where  one-half  of  the  body,  right 
or  left,  is  affected,  and  of  para-ancBsthesia  where  both  legs  or  both 
arms  are  affected  owing  to  a  lesion  of  the  spinal  cord  or  to  a 
symmetrical  affection  of  the  posterior  roots.  We  also  speak  of 
radial,  ulnar,  peroneal  anaesthesia,  &c.,  where  the  sensory  loss 
corresponds  to  the  distribution  of  a  single  peripheral  nerve. 

Hyperaesthesia. — Universal  hyperaesthesia  is  rare.  It  is 
chiefly  met  with  in  hysteria,  but  also  occurs  in  other  affections,  as 
in  strychnia-poisoning,  where  the  slightest  touch  may  suffice  to 
evoke  a  violent  spasm.  Hemi-hyperaesthesia  is  chiefly  found  in 
neurasthenic  and  hysterical  patients  and  may  be  associated  with 
other  hysterical  "  stigmata."  Thus  I  remember  the  case  of  a 
soldier  with  traumatic  hysteria  who  had  hemi-hyperaesthesia, 
accompanied  by  abnormal  widening  of  the  visual  fleld  and  by 
increased  acuity  of  smell,  taste,  and  hearing,  all  on  the  hyper- 
aesthetic  side  of  the  body. 

In  the  thalamic  syndrome,  hemi-hyperaesthesia  (or  excessive 
reaction)  to  temperature  and  pain,  sometimes  coexists  with  hemi- 
anaesthesia  (or  loss  of  sensation)  to  tactile  stimuli  and  with  impair- 
ment of  joint  sense,  loss  of  osseous  sense  and  astereognosis  in  the 
affected  limbs.     In  some  cases  the  pleasurable  sensation  produced 


ABNORMALITIES    OF    SENSATION  205 

by  a  warm  hand  applied  to  the  skin  of  the  affected  side  is  asso- 
ciated with  a  marked  accentuation  of  pleasure  ;  and  even  emotional 
conditions  of  pleasure  or  the  reverse  {e.g.  those  produced  by  music) 
may  be  accompanied  by  specially  intense  response  in  the  abnormal 
half  of  the  body.' 

Hypersesthesia  in  more  or  less  symmetrical  root-areas  of  the 
trunk  or  limbs,  due  to  irritation  of  the  posterior  roots,  is  not 
uncommon  in  diseases  causing  pressure  on  the  spinal  cord  or  its 
meninges,  as  in  caries  or  tumours  of  the  spine.  Here  the  hyper- 
sesthesia corresponds  to  the  area  supplied  by  the  uppermost  root 
involved,  and  is  usually  associated  with  anaesthesia  and  motor 
weakness  in  the  parts  below. 

Odd  irregular  areas  of  hypersesthesia,  which  do  not  cor- 
respond either  to  root-areas  or  to  the  distribution  of  peripheral 
nerves,  are  amongst  the  commonest  stigmata  of  hysteria.  Tender 
areas  are  particularly  common  over  hysterical  joints  and  over 
certain  vertebral  spines  in  hysteria,  and  we  frequently  notice  that 
the  lightest  touches  cause  severe  pain,  whereas,  when  the  patient's 
attention  is  diverted,  deep  pressure  on  the  same  spot  may  be 
painless.  Pressure  on  such  tender  spots  may  sometimes  excite  a 
hysterical  attack — "  hysterogenic  "  areas — and  in  other  cases  may 
restrain  or  stop  an  attack— "  hysterofrenic "  areas.  To  this 
subject  we  shall  return  when  discussing  the  diagnosis  of  hysteria. 

Next  in  frequency  after  hysterical  hypersesthesia  are  areas 
of  cutaneous  hypersesthesia  in  tabes.  Tactile  hypersesthesia  is 
specially  common  in  cases  with  gastric  or  other  visceral  crises, 
in  the  root-areas  corresponding  to  the  viscus  affected.  It  is 
also  common  in  the  areas  where  lightning-pains  are  felt,  and 
like  these  pains  it  may  be  one  of  the  earliest  evidences  of  the 
disease.  Thus  a  patient  with  incipient  tabes,  for  years  before 
he  reached  the  stage  of  ataxia,  was  so  hjrpersesthetic  around  the 
trunk  that  it  was  agony  for  him  to  pull  his  shirt  on,  or  to  sponge 
his  body  when  bathing.  Tabetic  hypersesthesia  may  occur  not 
only  on  the  trunk  but  also  on  the  limbs,  and  even  on  the  face. 
Hypersesthesia  is  specially  frequent  round  the  orbits  in  cases 
of  tabetic  ocular  palsies. 

Hypersesthesia  in  the  areas  of  peripheral  nerves  occurs  in  the 
true  neuralgias,  as  in  trigeminal  neuralgia,  where  the  neuralgic  area 
is  often  exquisitely  tender,  especially  over  the  foramina  of  exit  of 

1  Head  and  Holmes,  Brain,  1911,  pp.  134-135. 


206  NERVOUS   DISEASES 

the  various  branches.  The  patient  may  be  unable  to  wash  his  face 
for  weeks  at  a  time,  because  the  hghtest  touches  induce  a  par- 
oxysm of  neuralgia.  Localised  hjrpersesthesia  sometimes  precedes 
the  eruption  of  herpes  zoster,  and  may  persist  for  weeks  or  months 
after  the  eruption  has  passed  away.  Lastly,  we  may  mention 
the  hypersesthesia  of  the  hands  and  feet  in  multiple  neuritis,  in 
which  condition  there  is  often  present  a  degree  of  anaesthesia  also. 
The  coexistence  of  hyperalgesia  to  light  pressure  with  anaesthesia 
to  hght  touches  is  very  characteristic  of  alcoholic  neuritis. 

Paraesthesia,  or  perverted  sensation,  has  much  the  same  diag- 
nostic significance  as  hypersesthesia.  It  may  also  be  mentioned 
that  when  a  peripheral  cutaneous  nerve  is  in  process  of  recovery 
after  an  injury,  the  skin  often  passes  through  a  stage  of  paraesthesia 
before  normal  sensation  is  restored. 

Anaesthesia. — ^Universal  anaesthesia  of  the  skin  and  accessible 
mucous  membranes  to  all  forms  of  stimuli  is  exceedingly  rare, 
occurring  only  in  hysteria.  Fig.  87  shows  such  a  case  in  a  girl,  in 
whom  it  was  possible  to  push  pins  through  the  skin  on  both 
sides  of  the  body  without  causing  pain. 

Hemi-ansesthesia  always  indicates  a  central  affection.  In  every 
case  of  hemi-anaesthesia  we  must  determine  whether  the  disease  is 
functional  or  organic,  and  if  organic,  at  what  level  in  the  sensory 
tract  the  lesion  is  situated,  whether  in  the  cortex,  internal  capsule, 
optic  thalamus,  or  lower  down. 

Hysterical  hemi-ancesthesia  is  commoner  than  organic.  It  varies 
in  degree,  from  total  anaesthesia  down  to  the  slightest  degree  of 
blunting  of  sensation,  only  discoverable  on  comparison  of  the 
two  sides.  Not  uncommonly  it  tends  towards  the  "  segmental " 
type,  and  it  is  frequently  accompanied  by  other  hysterical 
stigmata,  especially  by  blunting  of  the  special  senses  on  the  hemi- 
anaesthetic  side,  particularly  by  concentric  contraction  of  the 
visual  field,  and  by  other  features  which  we  shall  study  later. 
We  should  remember  that  hysteria  sometimes  coexists  with 
organic  disease,  thereby  complicating  the  diagnosis. 

Organic  hemi-ancBsthesia  may  also  vary  in  its  degree,  from  slight 
to  severe  anaesthesia  ;  but  it  is  never  absolute  in  degree  as  in  some 
cases  of  hysteria.  It  is  generally  more  marked  on  the  limbs 
than  on  the  trunk  or  face,  and  more  intense  at  the  periphery  of 
a  limb  than  at  its  proximal  end.  It  is  never  marked  off  by  a 
sharp    line    running   across    the    limb,   as    is    the    "  segmental " 


ABNORMALITIES    OF    SENSATION 


207 


anaesthesia  of  hysteria,  but  fades  gradually  in  intensity  as  we 
pass  from  the  hand  to  the  shoulder.  A  degree  of  atopognosis  is 
always  present  in  organic  hemi-ansesthesia.  The  special  senses 
are  unaffected  (their  paths  probably  do  not  traverse  the  internal 


Fig.  87. — Universal  autesthesia  in  a  hj^sterical  patient.  Sterilised 
safety-pins  have  been  pushed  through  the  skin  on  both  sides 
without  producing  bleeding.  Hysterical  contracture  of  left  hand 
is  also  present. 

capsule),  with  one  exception,  namely  that  of  vision,  in  cases  in  which 
the  lesion  implicates  the  optic  radiations.  But  here  again  we  get 
a  homonymous  hemianopia,  unlike  the  hysterical  contraction  of 
the  visual  field  to  which  we  shall  refer  later. 

If  we  find  that  a  hemi-ansesthesia  is  organic  in  origin,  we  have 


208  NERVOUS    DISEASES 

then  to  determine  whetlier  the  lesion  is  cortical  in  situation  or 
whether  it  is  lower  : — in  the  thalamo- cortical  path,  in  the  optic 
thalamus  itself,  or  below  it.  In  cortical  hemi-anaestliesia  the  other 
signs  of  cortical  disease  will  aid  the  diagnosis.  The  presence  of 
monoplegia  rather  than  hemiplegia,  or  the  occurrence  of  Jack- 
sonian  fits,  will  point  to  a  cortical  localisation,  remembering 
that  the  cortical  sensory  areas  are  situated  in  the  post-central 
gyrus,  opposite  the  corresponding  motor  centres  in  the  pre- central 
gyrus.  Cortical  anaesthesia  is  specially  associated  with  untrust- 
worthiness  of  response  to  the  same  tactile  stimulus,  and  with 
abnormally  early  fatigue,  so  that  responses  to  touches  on  the 
affected  hand  rapidly  tend  to  disappear.  In  a  pure  cortical  lesion 
sensibility  to  pin-pricks  is  not  changed,  although  thermal  sensi- 
bility may  be  slightly  diminished.  But  the  most  frequent  sensory 
defects  produced  by  a  cortical  lesion  are  loss  of  joint-sense,  inability 
to  recognise  differences  in  the  weights  of  objects,  and  inability  to 
recognise  the  posture  of  the  affected  limb  in  space  when  the  eyes 
are  closed. ^  Cortical  anaesthesia  is  less  profound  than  thalamic, 
and  is  most  distinct  at  the  periphery  of  the  affected  hmb.  Indeed, 
in  cortical  anaesthesia  it  is  usual  for  the  trunk  to  be  little  or  not 
at  all  affected.  Marked  astereognosis  and  atopognosis  with  but 
slight  tactile  and  motor  loss  will  point  to  a  cortical  lesion,  probably 
in  the  post-Rolandic  region. 

Thalamic  hemi-anaesthesia,  generally  the  result  of  a  lesion  in 
the  postero- external  part  of  the  optic  thalamus,  is  never  mono- 
plegic  in  type,  but  always  affects  the  entire  half  of  the  body,  includ- 
ing the  trunk.  Hemi- anaesthesia  to  cotton- wool  touches,  from  a 
thalamic  lesion  is  associated,  as  we  have  seen,  with  paroxysmal 
pains  of  intolerable  severity  in  the  affected  limbs  and  side  of  the 
face,  and  often  with  excessive  sensibility  to  pain  and  temperature 
on  the  anaesthetic  side,  so  that  when  a  pin-point,  or  a  hot  or  cold 
object,  is  dragged  lightly  across  the  trunk  from  the  normal  to  the 
anaesthetic  side,  it  causes  excessive  discomfort  as  soon  as  it  crosses 
the  middle  line.  The  thalamic  syndrome  also  includes  hemi-ataxy 
of  the  limbs  and  spontaneous  choreiform  or  athetoid  movements. 
The  deep  reflexes  are  unaffected,  and  the  plantar  reflex  remains 
of  the  normal  flexor  type,  since  the  pyramidal  motor  path  is  intact. 
The  patient  often  gives  a  history  of  transient  motor  hemiplegia  at 
the  onset,  but  this  motor  weakness  rapidly  disappears  and  is  suc- 

^  Head  and  Holmes,  Brain,  1911,  vol.  xxxiv. 


ABNORMALITIES    OF    SENSATION  209 

ceeded  by  paroxysmal  pains  in  the  hemi-ansesthetic  limbs  and 
face.  The  intensity  of  thalamo-cortical  and  of  thalamic  anaes- 
thesia is  deeper  than  in  cortical  cases,  but  not  so  markedly  intensi- 
fied at  the  periphery  of  the  limbs.  It  is  associated  with  hemianopia 
if  the  lesion  extend  backwards,  or  with  motor  hemiplegia,  most 
marked  in  the  leg  (but  not  a  monoplegia),  if  the  lesion  extend 
forward  into  the  pyramidal  motor  path. 

We  may  also  have  sub-thalamic  hemi-anaestliesia  from  organic 
lesions  of  the  sensory  path  below  the  level  of  the  optic  thalamus  ; 
in  fact,  at  any  level  in  the  fillet  above  the  sensory  decussation  in 
the  medulla.  Such  lesions  are  no  longer  associated  with  hyper- 
sesthesia  to  painful  stimuli,  and  can  often  be  correctly  localised 
by  the  co-existence  of  other  signs.  Thus  a  unilateral  lesion 
in  the  dorsal  aspect  of  the  pons,  implicating  the  trigeminal  nerve  or 
nucleus,  together  with  the  remainder  of  the  sensory  fibres  belonging 
to  the  other  side  of  the  body,  will  cause  a  crossed  hemi-ancesthesia, 
i.e.  anaesthesia  of  the  face  on  the  side  of  the  lesion,  and  of  the  arm, 
trunk,  and  leg  on  the  opposite  side  (Fig.  13,  p.  19).  A  lesion  of 
the  sensory  path  in  the  medulla  below  the  level  of  the  trigeminal 
nerve,  must  be  more  widespread  laterally  to  produce  a  com- 
plete hemi-anaesthesia,  since  the  path  for  temperature  and  pain 
is  here  at  some  distance  from  the  tactile  path  (Fig.  12, 
p.  18). 

Anaesthesia  also  occurs  in  certain  lesions  of  the  spinal  cord.  We 
should  note,  however,  that  there  are  many  cord  diseases  in  which 
anaesthesia  is  absent,  such  as  progressive  muscular  atrophy, 
amyotrophic  lateral  sclerosis,  and  acute  anterior  poliomyehtis. 
Disseminated  sclerosis  also  is  a  disease  in  which  sensory  changes  are 
frequently  absent.  But  if  the  spinal  cord  be  destroyed  or  divided 
at  a  certain  transverse  level,  whether  by  trauma  or  by  disease 
such  as  acute  softening,  whereby  sensory  as  well  as  motor  paths  are 
interrupted,  all  the  sensory  impressions  ascending  in  the  posterior 
and  lateral  columns  (Figs.  9  and  11,  pp.  12  and  15)  will  be  lost 
below  the  level  of  the  lesion.  We  then  have  a  para-ancesthesia,  the 
upper  limit  of  which  corresponds  with  that  of  the  highest  sensory 
root  affected.  The  anaesthesia  of  a  total  transverse  lesion  impH- 
cates  all  forms  of  sensation,  both  superficial  and  deep.  And  since 
in  many  of  these  cases  there  are  irritative  or  inflammatory  pro- 
cesses affecting  the  roots  immediately  above  the  area  of  destruc- 
tion, it  not  unfrequently  happens  that  there  is  a  narrow  zone 

0 


210  NERVOUS    DISEASES 

of    pargesthesia     or    of    hypersestliesia    immediately    above    the 
ansesthetic  area. 

In  cases  in  which  the  cord  is  gradually  compressed  by  pro- 
gressive disease  in  the  meninges  or  vertebrae,  there  is  usually 
a  progressive  paraplegia  with  the  usual  alteration  of  reflexes. 
Here  anaesthesia  appears  late  in  the  disease,  being  preceded  by 
spontaneous  subjective  sensations  or  dyscesthesice,  after  which 
hypersesthesia  appears,  and  last  of  all  anaesthesia.  Moreover, 
in  compression-paraplegia  the  lower  sacral  root-areas  are  usually 
less  deeply  anaesthetic  than  the  areas  above. 

When  a  cord  lesion  is  incomplete  in  its  transverse  extent,  certain 
forms  of  sensation  may  escape.     Thus  unilateral  lesions  of  the  cord 

produce  Brown-S^quard  paralysis.  Most 
commonly  this  is  the  result  of  a  stab  or 
bullet-wound,  but  it  may  also  be  caused 
by  softenings  or  growths.  Or  a  lesion 
which  was  originally  more  extensive,  e.g. 
a  haemorrhage,  may  clear  up  so  as  to 
become  a  unilateral  one.  In  the  typical 
Brown-Sequard  syndrome,  as  will  be 
seen  from  Figs.  11  and  14,  there  are  on 
the  side  of  the  lesion  the  well-known 
Fig.  sllsyriDgomyeHa,  indi-  "lo^or  and  vaso-motor  paralyses,  to- 
cating  area  of  thermo-anajs-  gether    with    loss  of    sensation   in  the 

thesia  and  analgesia  in  the    •    •    ,  -,  i  i     i  c       ■^ 

patient  shown  in  Fig.  86.  joi^^^s  ^nd  muscles  and  loss  of  vibra- 
tion-sense, whilst  on  the  opposite  side 
there  are  thermo- anaesthesia,  analgesia  and  some  tactile  anaes- 
thesia. In  thermo -anaesthesia  from  cord  lesions,  the  areas  of 
anaesthesia  to  cold  and  to  heat  are  sometimes  co -extensive.  But 
this  is  not  always  so  ;  sensibility  to  heat  may  be  abolished  without 
loss  of  sensibility  to  cold,  or  vice  versa,  or  the  areas  of  loss  to  heat 
and  to  cold  may  differ  widely  in  extent.  If  the  lesion  be  above 
the  lumbar  enlargement,  as  is  generally  the  case,  the  motor 
paralysis  is  of  the  upper  neurone  type,  with  spasticity,  increased 
deep  reflexes  and  an  extensor  type  of  plantar  reflex.  If,  as  some- 
times happens  in  stab-wounds,  the  lesion  destroys  the  most  lateral 
region  of  the  cord  but  does  not  quite  reach  the  middle  line, 
thereby  sparing  the  postero -internal  column,  the  deep  structures 
on  the  side  of  the  lesion  preserve  their  sensibility.  In  any  case, 
on  the  side  of  the  lesion,  a  narrow  zone  of  anaesthesia  exists, 


ABNORMALITIES    OF    SENSATION  211 

corresponding  to  the  posterior  root-fibres  cut  across  at  the  level 
of  the  lesion.  And,  in  cases  with  an  abrupt  onset  there  is,  above 
the  anaesthesia,  a  zone  of  hypersesthesia  from  irritative  root- 
changes. 

Dissociated  anaesthesia,  often  without  motor  paraplegia,  is  char- 
acteristic of  disease  in  the  region  of  the  posterior  cornua  of  the  cord 
or  in  the  substantia  gelatinosa  of  the  medulla,  as  in  syringomyelia 
and  syringobulbia,  in  which  analgesia  and  thermo-ansesthesia  occur, 
together  with  loss  of  vibration-sense,  corresponding  to  the  area 
of  spinal  cord  affected,  wher:as  tactile  sensation  remains  unim- 


FlG.  89. — Syringomyelia  with  arthropathy  of  right  shoulder-joint 
and  scoliosis. 

paired  (see  Fig.  88).  The  patient  often  burns  his  fingers  accidentally 
without  pain,  and  he  may  develop  painless  whitlows  in  his 
analgesic  fingers — so-called  Morvan's  disease.  He  may  also  have 
spontaneous  disintegrations  in  joints,  with  fractures  and  osteophytic 
or  destructive  changes  in  the  articular  ends  of  the  bones.  In 
most  cases  of  syringomyelia  there  also  is  some  atrophy  of  the 
anterior  cornua ;  therefore  we  should  be  on  the  look-out  for  a 
coexisting  muscular  atrophy  of  spinal  type,  involving  especially 
the  small  muscles  of  the  hands.  If  the  pyramidal  tracts 
become  involved  in  syringomyelia,  a  spastic  paraplegia  is  super- 
added, and  sooner  or  later  a  degree  of  scoliosis  or  even  kypho- 
scoliosis develops  (Fig.  89). 


212 


NERVOUS    DISEASES 


But  unilateral  cord  lesions  and  syringomyelia  are  not  the  only 
diseases  which  produce  dissociated  anaesthesia.  A  small  lesion 
such  as  an  area  of  softening  or  of  new  growth,  in  the  ponto-cerebellar 
angle  of  the  pons,  at  the  level  of  the  auditory  nerve,  will  cause 
deafness  of  the  same  side  with  analgesia  and  the rmo -anaesthesia 
of  the  opposite  side,  tactile  sensation  being  unaffected.  If  the 
cerebellar  peduncle  be  involved,  there  will  be  cerebellar  phenomena 
also,  such  as  we  have  already  studied. 

Tabetic  anaesthesia  is  the  commonest  of  all  organic  ansesthesise. 
In  this  disease  the  sensory  loss  tends  to  follow  fairly  closely  the  dis- 
tribution of  the  posterior  roots  affected 
by  the  tabetic  process.  Thus  it  is  com- 
moner in  the  lower  limbs  than  in  the 
upper.  Joint-sense  and  vibration-sense 
usually  become  impaired  earlier  than 
cutaneous  sensations,  whilst  analgesia 
precedes  tactile  anaesthesia.  In  the  upper 
limbs  the  fingers  on  the  ulnar  side  of 
the  hand  are  usually  affected  earher  than 
the  other  digits,  and  there  is  often 
a  strip  of  analgesia  running  longitudin- 
ally along  the  inner  side  of  the  whole 
upper  hmb,  corresponding  to  the  eighth 
cervical  and  first  thoracic  roots  (Fig.  90). 


Fig.  90. — Early  tabes,  show- 
ing "cuirass"  of  subjective 
girdle-feeling  (dotted  area) 
with  zone  of  cutaneous 
hyperassthesia      below      the  .  i     i  •     t 

cuirass,  passing  up  between  In  many  tabetics  the  ulnar  nerve  behmd 
itshmitsposterioriy (crosses).  ^-^^  elbow  loses  its  normal  sensitivcness 


Analgesic  areas  (horizontal 
shading)  in  upper  limbs  (Og 
and  Th^  roots)  and  in  lower 
limbs  (L4,  L5,  and  Sj  roots). 


on  pressure — ^Biernacki's  sign.  And  on 
the  trunk  it  is  common  to  find  a  broad 
of    analgesia,    and  sometimes   of 


zone 


tactile  anaesthesia  as  well,  the  upper  border  of  which  is  at 
the  level  of  the  second  ribs  in  front.  This  zone  is  often  incom- 
plete laterally  or  posteriorly,  just  as  the  subjective  "  cuirass " 
sensation  may  be.  Analgesia  of  the  glans  penis  is  another  early 
sign  of  tabes,  also  loss  of  the  normal  tenderness  of  the  testicle 
on  pressure.  Acute  inflammatory  affections  of  the  viscera,  which 
in  an  ordinary  individual  are  highly  painful,  may  in  certain  tabetic 
patients  run  their  course  painlessly  and  even  without  rigidity  of  the 
superjacent  muscles.  Thus  a  tabetic  patient  may  have  acute 
pleurisy  without  pain,  or  an  acute  appendicitis  may  progress  pain- 
lessly to  perforation  and  to  diffuse,  fatal  peritonitis.     These  facts 


ABNOKMALITIES    OF    SENSATION 


213 


are  probably  to  be  explained  by  the  presence  of  tabetic  degenera- 
tion in  the  grey,  afferent,  rami  communicantes  leading  from  the 
sympathetic  to  the  posterior  root  ganglia.  Tendinous  analgesia, 
on  pinching  the  tendo  Achillis  [Ahadie's  sign),  is  also  present 
in  the  majority  of  tabetic  patients.  But  tabetic  anaesthesia  is  not 
always  sharply  limited  to  root  areas,  and  we  should  seek  for  con- 
firmatory evidence  of  the  disease  in  the  pupils,  deep  reflexes,  cerebro- 
spinal fluid,  &c. 

Anaesthesia  in  peripheral  nerve  palsies  of  sensory  or  mixed 
nerve-trunks,  is  of  course  confined  to  the  distribution  of  the 
affected  nerve  or  nerves.     If  a  pure  cutaneous  nerve  be  paralysed 


Fig.  91. — From  a  case  of  multiple 
neuritis,  showing  "glove"  and 
"  sock"  areas  of  anaesthesia. 


Fig.  91a.— From  another  case  of 
peripheral  neuritis,  showing 
"  glove  "  and  "  stocking  "  areas 
of  cutaneous  paresthesia. 


we  have  loss  of  cutaneous  sensations,  both  "  epicritic  "  and  "  proto- 
pathic,"  whilst  the  deep  sensibility  in  muscles,  tendons  and  bones 
is  still  preserved  (see  p.  15).  The  area  of  cotton-wool  anaesthesia 
in  a  peripheral  nerve  lesion  is  always  more  extensive  than  the  area 
of  analgesia  to  pin-pricks.  But  as  we  ascend  the  nerve-trunk  in  a 
proximal  direction,  the  two  areas  become  more  nearly  co-terminous, 
untn  in  a  posterior  root-lesion  the  area  of  loss  to  pin-pricks  actually 
exceeds  that  of  anaesthesia  to  cotton-wool  touches.  As  Head  has 
put  it,  the  nearer  the  lesion  lies  to  the  central  nervous  system 
the  more  extensive  and  definite  is  the  loss  to  pin-pricks  ;  the  nearer 
to  the  periphery,  the  greater  is  the  loss  to  cutaneous  touch  with 
cotton-wool  stimuli. 

If  a  mixed  nerve-trunk  be  paralysed,  muscular  paralysis  with 
atrophy  is  added  to  anaesthesia,  not  only  of  cutaneous  but  also  of 


214 


NERVOUS   DISEASES 


deep  sensibility  in  tlie  corresponding  bones,  joints  and  tendons, 
and  the  diagnosis,  as  a  rule,  presents  no  difficulties.  It  must  be 
borne  in  mind  that  as  a  mixed  nerve  recovers  from  its  paralysis, 
sensation  usually  returns  before  motor  power  and  protopathic 
sensations  recover  before  epicritic. 

The  anaesthesia  following  an  attack  of  herpes  zoster  sometimes 
lasts  for  a  considerable  time  after  the  eruption  has  disappeared. 

In  the  anaesthesia  of  multiple  neu- 
ritis, whether  resulting  from  alcohol, 
diphtheria,  diabetes,  septic  poisoning,  or 
other  causes,  the  disease  is  generally 
bilateral  and  symmetrical,  affecting 
hands  or  feet  or  both.  Subjective  ting- 
ling sensations  usually  precede  the 
anaesthesia,  which  is  of  the  "  glove " 
and  "sock"  variety,  not  marked  off 
sharply  as  in  the  "  segmental "  anaes- 
thesia of  hysteria,  but  shading  off 
gradually  at  the  upper  margin  (see 
Figs.  91  and  91a).  Most  cases  have 
also  some  superadded  motor  weakness  in 
the  form  of  drop-foot  and  drop-wrist. 

The  anaesthesia  of  leprous  neuritis  is  often  curiously  patchy  and 
asymmetrical  (see  Fig.  92).  It  is  associated  with  palpable  thicken- 
ing of  the  nerve-trunks  and  often  with  trophic  changes  in  the 
skin,  &c.  (see  later,  p.  309). 

Lead  paralysis  differs  from  ordinary  peripheral  neuritis  in  being 
entirely  a  motor  palsy,  free  from  sensory  changes,  and  whilst 
affecting  the  muscles  innervated  by  the  musculo-spiral  nerve,  it 
usually  leaves  the  supinator  longus  unimpaired.  Moreover,  the 
extensor  communis  is  less  severely  paralysed  than  the  extensor 
indicis  and  extensor  minimi  digiti. 


Fig.  92. — Ancesthesia  in  lep- 
rous neuritis. 


CHAPTEH   XIII 

ORGANIC   MOTOR   PARALYSIS   OF   UPPER   NEURONE   TYPE 

In  the  investigation  of  the  various  motor  palsies,  apart  from  those 
affecting  the  cranial  nerves  which  we  have  already  studied,  we 
should  proceed  in  a  definite  order. 

We  commence  by  inspection  of  the  palsied  limb  or  limbs,  noting 
the  posture  of  the  limb,  the  presence  or  absence  of  local  mus- 
cular atrophy  or  hypertrophy,  the  existence  of  wounds,  swellings, 
or  other  deformities.  We  then  proceed  to  palpation  of  the  bones 
and  joints,  following  their  outlines  and  testing  their  range  of  passive 
movement,  so  as  to  discover  whether  the  deficiency  of  active  move- 
ment may  not  be  due  to  mechanical  causes,  such  as  fractures,  dis- 
locations, ankyloses,  adhesions  or  inflammations  of  bones  or  joints, 
and  so  on.  Thus  in  the  case  of  a  semi-comatose  lady,  whom  I  saw 
within  a  few  hours  after  a  carriage  accident,  there  was  apparent 
inabihty  to  move  the  left  arm  or  leg.  This  might  have  suggested 
a  lesion  of  the  right  cerebrum  producing  hemiplegia,  but  a  pre- 
liminary investigation  of  the  bones  showed  that  the  left  femur  and 
left  clavicle  were  broken.  It  was  therefore  unnecessary  to  diagnose 
an  intra-cranial  lesion  of  the  pyramidal  tract,  especially  as  the 
plantar  reflexes  were  normal  on  both  sides.  The  result  proved 
the  correctness  of  this  view. 

We  should  also  observe  whether  the  muscles  of  the  affected 
part  are  rigid,  stiff  and  spastic,  or  whether  they  are  loose,  relaxed 
and  flaccid. 

Lastly,  we  proceed  to  investigate  the  patient's  powers  of  volun- 
tary movement  of  the  affected  limb.  In  doing  this,  it  is 
not  enough  to  tell  the  patient  in  general  terms,  to  "  move  the 
arm,"  and  so  on.  We  should  test  each  joint  and  each  movement 
separately,  fixing  the  proximal  part  of  the  limb  and  instructing 
the  patient  to  perform  various  movements : — flexion,  extension, 
rotation    inwards  and   outwards,    &c.,    separately  and  distinctly, 

215 


216  NERVOUS    DISEASES 

Thus,  for  example,  when  we  direct  a  patient  to  pronate  his  fore- 
arm, we  must  fix  the  humerus  and  see  that  he  does  not  abduct 
the  shoulder  to  make  up  for  deficiency  in  pronation.  To 
determine  whether  a  particular  muscle  is  taking  part  in  a  move- 
ment or  not,  sometimes  requires  very  close  observation,  not 
only  by  inspection  but  by  palpation  of  the  muscle  or  of  its 
tendon.  But,  as  Beevor  has  remarked,^  the  physician  "  must 
avoid  the  error  of  assuming  that  the  tightening  of  a  tendon  from 
the  stretching  of  a  passive  muscle  is  evidence  of  contraction  of 
the  muscle." 

Suppose  that  a  particular  movement  of  a  limb  is  deficient, 
we  estimate  the  deficiency  in  different  ways,  according  to  its  degree. 
If  the  weakness  is  shght,  we  detect  it  by  interposing  some  resist- 
ance, so  as  to  load  the  muscles.  This  is  accompHshed  either  by 
means  of  weights,  or,  in  the  case  of  the  hand,  by  making  the 
patient  squeeze  our  hand  or  compress  an  oval  spring-dynamometer, 
or,  in  the  case  of  the  leg,  by  holding  the  limb  down  and  making 
him  elevate  it  against  resistance. 

If  the  weakness  is  more  marked,  it  can  be  detected  without 
loading  the  muscles.  The  weight  of  the  distal  part  of  the  limb 
may  in  itself  be  too  much  for  the  muscles  to  lift,  as,  for  example, 
in  cases  of  drop-wrist  and  drop-foot,  due  to  weakness  of  the  ex- 
tensors of  the  wrist  and  dorsiflexors  of  the  foot.  But  even  in 
these,  a  minimal  degree  of  voluntary  contraction  may  perhaps 
still  be  present,  and  can  still  be  detected  by  placing  the  Hmb  pas- 
sively in  such  a  posture  that  its  own  weight  is  no  longer  a  factor, 
e.g.  by  testing  the  extensors  of  the  wrist  with  the  forearm  midway 
between  pronation  and  supination,  or  testing  the  movements  of 
the  elbow  by  passively  abducting  the  upper  arm  and  getting  the 
patient  to  flex  and  extend  his  elbow  in  a  horizontal  plane.  Or  we 
may  even  observe  the  Hmb  when  it  is  supported  on  all  sides  by 
water,  as  in  a  warm  bath.  In  this  way  we  may  detect  minimal 
movements.  And  in  such  cases  we  watch  carefully,  not  only  for 
movement  of  the  joint,  but  for  contraction  of  the  tendons  of  the 
muscles  concerned.  These  latter  may  sometimes  be  felt  to  con- 
tract, when  they  are  too  feeble  to  overcome  the  inertia  of  the 
joint. 

By  inspection  and  palpation  we  also  note  whether  in  the  affected 
limb  the  muscles  are  normal  in  volume  and  firmness,  whether  some 

1  Croonian  Lectures,  1904,  p.  4. 


PARALYSIS    OF    UPPER    NEURONE    TYPE         217 

are  enlarged  and  stronger  than  usual — hypertro'phy — or  whether 
some  are  diminished  in  size — atrophy,  so  that  there  is  flattening, 
or  even  hollowing,  in  place  of  the  normal  muscular  contour.  In 
some  cases,  an  apparent  increase  in  volume  is  accompanied 
by  weakness  of  the  enlarged  muscles — so-called  fseudo-hyper- 
trophy. 

If  a  muscle  be  atrophied,  its  electrical  reactions,  both  to 
faradic  shocks  and  to  the  continuous  galvanic  current,  should  be 
investigated.  The  reactions  may  be  normal,  or  they  may  be 
merely  quantitatively  diminished.  Or  they  may  be  quahtatively 
altered,  as  in  the  "  reactions  of  degeneration  "  (see  later,  p.  426). 
Or  they  may  be  "  mixed,"  when  some  fibres  of  the  muscle 
are  normal,  whilst  others  intermingled  with  them  are  degener- 
ated. 

Reaction  of  a  muscle  to  direct  percussion  is  sometimes  of  value. 
This  phenomenon  consists  in  a  contraction  of  the  whole  bundle 
of  muscle-fibres  in  their  entire  length.  Response  to  direct 
mechanical  excitation  often  persists  when  the  deep  reflexes  are 
lost ;  thus,  for  example,  when  the  knee-jerk  is  absent  in  tabes 
or  peripheral  neuritis,  the  quadriceps  still  responds  to  direct  tapping. 
In  most  cases  of  lower  motor  neurone  lesion,  this  mechanical 
irritability  of  the  muscle-fibres  is  increased  but  the  contraction  is 
more  flickering  than  in  a  healthy  muscle.  In  muscular  dystrophy, 
the  mechanical  irritability  is  lost  in  the  aflected  muscles.  In 
certain  patients,  especially  on  percussing  the  pectorals  or  other 
flat  muscles  of  the  chest,  we  may  observe  a  wave  of  contraction 
dashing  outwards  suddenly  in  both  directions  from  the  point 
of  percussion,  along  the  course  of  the  muscular  fibres,  and  imme- 
diately followed  by  a  temporary  small  muscular  swelling  at 
the  point  of  percussion.  This  phenomenon  is  called  myoidema ; 
it  is  common  in  pulmonary  tuberculosis,  but  occurs  also  in  many 
other  wasting  conditions  not  associated  with  muscular  paralysis, 
and  need  not  detain  us  further. 

The  term  paralysis,  when  applied  to  voluntary  muscles, 
signifies  loss  of  the  power  of  voluntary  contraction,  due  to  inter- 
ruption, functional  or  organic,  in  any  part  of  the  motor  path,  from 
the  cerebral  cortex  down  to  and  including  the  muscle-fibre.  This 
latter  part  of  the  definition  is  necessary  so  as  to  exclude  such 
cases  as  ankylosed  joints,  in  which  movement  is  impossible  from 
mechanical    reasons  without  true  paralysis.       Strictly  speaking, 


218  NERVOUS   DISEASES 

paralysis  is  total  loss  of  voluntary  motor  power,  lesser  degrees  of 
irapairment  being  called  paresis.  But  we  often  employ  the 
term  paralysis  to  include  partial  as  well  as  complete  loss  of 
power. 

The  distribution  of  motor  weakness  differs  according  to  the 
site  of  the  lesion  of  the  motor  path.  Thus  in  a  unilateral 
brain  lesion,  there  is  usually  paralysis  of  one  side  of  the  body, 
including  the  face,  trunk  and  Hmbs.  This  is  termed  hemi- 
flegia.  A  bilateral  cerebral  lesion  produces  diplegia  or  double 
hemiplegia,  the  limbs  on  both  sides  of  the  body  being  affected. 
Paralysis  of  a  single  Hmb  resulting  from  a  cerebral  lesion  is 
termed  cerebral  monoplegia.  Spinal  or  peripheral  monoplegia  is 
less  common. 

Paralysis  of  the  limbs  resulting  from  a  lesion  of  the  spinal  cord 
is  most  commonly  bilateral — paraplegia — and  usually  affects  the 
legs  alone ;  but  if  the  lesion  be  in  the  cervical  region,  it  affects 
both  arms  and  legs.  It  must  be  distinguished  from  a  cerebral 
diplegia,  in  which  the  face  is  sometimes  also  affected.  In  rare 
cases  both  arms  may  be  paralysed  from  a  spinal  lesion,  with  httle 
or  no  affection  of  the  legs  ;  this  is  brachial  paraplegia.  A  uni- 
lateral spinal  lesion  may  also  cause  a  monoplegia,  but  this  is  un- 
common. The  term  crossed  or  alternate  hemiplegia  means  that  as 
a  result  of  a  single  lesion  there  is  paralysis  of  some  parts  on  the 
right  side  and  of  others  on  the  left.  For  example,  a  lesion  in 
the  right  side  of  the  pons  at  the  level  of  the  facial  nerve  will 
cause  paralysis  of  the  right  side  of  the  face  and  of  the  left 
arm  and  leg.  There  are,  of  course,  other  varieties  of  crossed 
paralysis. 

When  paralysis  is  due  to  a  lesion  of  a  peripheral  nerve,  it 
may  either  be  asymmetrical,  when  the  motor  weakness  is  limited 
to  one  or  more  nerve-trunks,  as  in  most  traumatic  nerve-palsies, 
or  more  commonly  bilateral  and  symmetrical,  as  in  the  various 
forms  of  toxic  neuritis,  affecting  either  the  upper  or  lower  or  all 
four  Hmbs. 

If  paralysis  be  due  to  primary  affection  of  the  muscles 
themselves,  as  in  the  myopathies,  its  distribution  is  usually 
bilateral,  and  it  affects  all  four  limbs  and  sometimes  even  the 
face. 

We  must  remember  that  it  is  not  uncommon  to  meet  with 
multiple  lesions  in  a  single  case  ;   yet,  in  diagnosis,  it  should  always 


PARALYSIS   OF    UPPER   NEURONE   TYPE         219 

be    our    endeavour  to  try   to  account  for  all  the  symptoms  by  a 
single  lesion. 

Suppose,  then,  that  a  patient  is  suffering  from  motor  paralysis 
(mechanical  impediments  having  been  excluded),  the  first  ques- 
tion is — Is  the  paralysis  functional  or  organic?  If  it  is  organic, 
we  proceed  to  the  further  questions — Where  is  the  lesion  situated  ? 
(anatomical  diagnosis),  and  what  is  its  nature  ?  (pathological 
diagnosis). 

Is  the  Paralysis  Functional  or  Organic  ?— Sometimes  the 
distinction  between  functional  and  organic  motor  paralysis  is 
easy ;  at  other  times  it  is  a  matter  of  considerable  difficulty. 
Thus  cases  of  early  disseminated  sclerosis  are  particularly  liable 
to  be  mistaken  for  hysteria.  Moreover,  it  is  possible  to  have 
a  combination  of  functional  and  organic  disease  in  the  same 
patient. 

More  detailed  consideration  of  the  diagnostic  features  of 
hysteria  will  be  postponed  till  a  later  chapter  (see  p.  383),  and  we 
shall  only  here  refer  to  some  of  the  main  features  which  enable  us 
to  decide  that  a  case  is  organic  rather  than  functional.  Firstly,  the 
history  of  the  case  often  guides  us ;  for  instance,  functional 
paralysis  frequently  follows  an  emotional  shock  or  a  prolonged 
mental  strain,  whereas  traumatism,  as  in  railway  accidents,  is 
equally  liable  to  cause  functional  or  organic  disease. 

There  are  two  classes  of  signs  and  symptoms  which  point 
to  functional  rather  than  to  organic  disease — firstly,  the  absence 
of  characteristic  signs  of  organic  disease,  and  secondly,  the 
presence  of  certain  phenomena  pecuhar  to  functional  disease. 
Muscular  atrophy,  while  much  less  frequent  in  functional  than 
in  organic  palsies,  is  not  pathognomonic  of  organic  disease. 
Thus  Fig.  206  (p.  404)  shows  a  case  of  hysterical  monoplegia 
with  extensive  muscular  atrophy,  a  rare  combination.  But  the 
electrical  reactions  of  degeneration  are  never  obtained  in  functional 
paralysis.  Their  presence  signifies  undoubted  organic  disease, 
somewhere  in  the  spino-muscular  neurone.  Paralysis  of  a  single 
muscle  is  pathognomonic  of  organic  disease :  it  never  occurs  in 
functional  paralysis,  which  affects  whole  muscle-groups  or,  to 
speak  more  accurately,  whole  movements.  To  sum  up,  then, 
the  diagnosis  between  functional  and  organic  paralysis  is  easy  if 
the  organic  palsy  is  of  the  lower  motor  neurone  type.  It  is 
chiefly  when  the  organic  lesion  is  in  the  upper  or  cortico- spinal 


220  NERVOUS    DISEASES 

neurone  that  difficulty  is  liable  to  occur,  i.e.  in  cases  in  which,  there 
is  little  or  no  muscular  atrophy,  and  where  the  electrical  re- 
actions are  normal.  In  such  cases  the  presence  or  absence  of 
other  hysterical  stigmata  is  of  great  value. 

A  valuable  sign  of  organic  as  contrasted  with  hysterical  hemi- 
plegia is  Babinski's  combined  -flexion  of  the  hip  and  trunk,  a 
phenomenon  almost  invariably  present  in  organic  cases.  To  elicit 
this  the  patient  lies  flat  on  his  back  on  a  smooth  hard  surface,  such 
as  a  table  or  the  floor,  with  his  arms  crossed  in  front  of  his  chest 
and  the  legs  not  allowed  to  touch  each  other.  We  then  ask  him 
to  sit  up  without  using  his  arms.  (See  Fig.  93.)  As  he  does  so,  the 
organically  paralysed  lower  limb  becomes  flexed  at  the  hip  and  the 
heel  is  raised  from  the  surface.  Meanwhile  the  shoulder  on  the 
healthy  side  is  carried  forwards,  as  if  to  counterpoise  the  contra- 
lateral lower  limb.  In  hysterical  hemiplegia  this  sign  is  absent,  and 
the  hysterically  paralysed  limb  remains  unraised.  Another  useful 
test  to  distinguish  between  organic  and  functional  paralysis  is  the 
phenomenon  of  Grasset  and  Gaussel,^  which  is  also  confined  to 
organic  cases.  This  consists  in  inability  on  the  part  of  the  organically 
hemiplegic  patient  to  raise  both  lower  limbs  simultaneously  from  the 
surface  when  lying  down  as  before,  although  he  is  still  able  to  lift 
either  lower  limb  separately.  The  reason  for  this  peculiarity  is  that 
in  organic  hemiplegia  the  patient,  when  he  tries  to  lift  both  lower 
limbs  at  once,  is  unable  to  fix  the  pelvis.  In  testing  far  this  sign, 
we  must  be  careful  to  see  that  the  two  legs  do  not  touch  each 
other,  since  the  patient  often  tends  involuntarily  to  help  up  the 
paralysed  limb  by  means  of  the  sound  one.  Of  course,  the* sign  is 
only  present  in  cases  of  incomplete  hemiplegia.  Another  way  of 
showing  the  same  phenomenon  is  to  direct  the  patient  to  raise  the 
lower  limb  of  the  paralysed  side  and  hold  it  in  the  air.  If  we  now 
grasp  the  sound  leg  and  raise  it  up,  the  other  limb  at  once  falls 
down  again,  because  the  pelvis  cannot  be  steadied  by  the  muscles 
on  the  paralysed  side.  On  the  other  hand,  if  the  patient  first 
raises  the  sound  leg  and  we  then  passively  lift  the  paralysed  one, 
the  sound  limb  still  remains  in  the  air,  the  pelvis  remaining 
fixed  by  the  non-paralysed  muscles  of  the  healthy  side.  In 
hysteria  there  is  no  such  difference  between  the  separate  and 
the  simultaneous  raising  of  the  legs. 

1-  Revue  neurologiquc,  1905,  p.  881 


PARALYSIS    OF    UPPER    NEURONE    TYPE        221 

In  some  cases  of  spastic  paraplegia  the  rigidity  of  the  lower 
limbs  is  of  diagnostic  value.  Thus  when  we  passively  lift  one 
lower  limb  off  the  bed  and  find  that  the  other  lower  limb  is 
thereby  lifted  up  as  well,  we  may  be  practically  certain  that  the 
rigidity  and  paralysis  are  organic  and  not  functional. 

A  careful  study  of  the  reflexes  is  also  of  the  utmost  importance. 
The  presence  of  an  extensor  plantar  reflex  in  a  patient  beyond 
the'^age  of  infancy  is  pathognomonic  of  organic  disease  (see  later, 
p.  333).      The  deep  reflexes,  although  they  may  be  exaggerated 


Fig.  98. — Case  of  left  hemiplegia,  showing  phenomenon  of  comhhud  flexion 
^-„  of  hip  and  trunh  on  attempting  to  sit  up  without  using  arms. 


both  in  functional  and  in  organic  paralysis,  are  usually  normal 
in  functional  cases.  True  ankle-clonus  of  organic  disease  is 
generally  readity  distinguished  from  the  "  pseudo-clonus "  of 
functional  disease.  Absence  of  the  deep  reflexes  may  occur  in 
organic,  never  in  functional  disease. 

Incontinence  of  the  bladder  and  rectum  is  not  uncommon  in 
organic  diseases  of  the  spinal  cord  and  brain,  but  practically  never 
occurs  in  functional  paraplegia. 

Where  is  the  Organic  Lesion? — Suppose  we  have  come  to 
the  conclusion  that  the  patient's  motor  paralysis  is  organic  in  type, 
we  have  to  ask  ourselves  at  what  point  in  the  motor  path  the 
lesion  is  situated.  First,  we  must  decide  whether  the  lesion  is  in 
the  upper  (cortico-spinal),  or  in  the  lower  (nucleo-muscular)  motor 


222  NERVOUS    DISEASES 

neurone.     The  distinctive  characters  of  these  two  types  are  as 
follows  : — 

ORGANIC  MOTOR  PARALYSIS. 

Upper  (cortico-spinal)  Neurone.        Lower  (spino-muscular)  Neurone. 
Supra-Nuclear  Paralysis.  Nuclear    and    Infra -Nuclear 

Paralysis. 

1.  Diffuse     muscle-groups      affected,      1.  Individual  muscles  may  beaffected. 

never  individual  muscles. 

2.  Spasticity   and   hyper-tonicity   of      2.  Flaccidity  and  atonicity  of  para- 

paralysed  muscles.  lysed  muscles. 

3.  May  have  superadded  "associated      3.  No  "associated  movements." 

movements "    (synkinesise)    on 
attempted  voluntary  movement. 

4.  No  muscular  atrophy,  except  from      4.  Atrophy  of  paralysed  muscles. 

disuse. 

5.  Electrical  reactions  normal.  5.  Reactions  of  degeneration. 

6.  Deep  reflexes  in  paralysed  limbs      6.  Deep  reflexes  of  paralysed  muscles 

present,  and  usually  increased.  diminished,  and  often  absent. 

7.  If  foot  affected,  plantar  reflex  ex-      7.  Plantar   reflex,   if    present,    is   of 

tensor  in  type.  normal     flexor     type     (unless 

flexors   of  toes  are  themselves 
paralysed). 

Let  us  consider  some  of  these  points  more  in  detail.  Paralysis 
due  to  an  upper  neurone  lesion  never  affects  an  individual  muscle, 
but  always  a  diffuse  muscular  group.  The  converse,  however,  is 
not  true,  and  we  must  remember  that  even  a  lower  neurone  lesion 
may  produce  a  diffuse  paralysis,  where  a  series  of  adjacent  nerves 
or  nuclei  are  affected.  But  if  individual  muscles  are  picked 
out  by  paralysis,  the  adjoining  or  intermingled  muscles  being 
perfectly  normal,  the  cause  is  certainly  a  nuclear  or  infra-nuclear 
lesion. 

Paralysis  from  a  cortico-spinal  lesion  is  rarely  permanently 
complete.  It  is  more  often  a  paresis  than  an  absolute  paralysis. 
In  this  respect  it  differs  from  the  total  palsy  of  a  spino-muscular 
lesion. 

Spasticity  of  the  paralysed  nmscles  in  supra-nuclear  lesions 
does  not  set  in  immediately  after  the  onset  of  a  sudden  lesion, 
but  usually  develops  gradually  in  the  course  of  from  one  to 
three  months.  Thus  in  a  typical  supra-nuclear  lesion,  as,  for 
example,  in  apoplexy,  there  is  an  initial  period  of  flaccidity, 
gradually  replaced  by  the  so-called  "  late  rigidity."  The  degree 
of  this  spasticity  varies  in  different  cases.  We  estimate  it  by 
moving  the  patient's  joints  passively,  and  comparing  their  resistance 
with  that  of  a  healthy  limb. 


PARALYSIS    OF    UPPER    NEURONE    TYPE        223 

Patients  with  motor  paresis  due  to  cortico-spinal  lesions  not 
uncommonly  show  superadded  "  associated  movements "  or  syn- 
kinesicB  on  attempting  to  execute  a  voluntary  movement  with  the 
paresed  limb.  Thus,  for  example,  if  the  patient  tries  to  draw  up 
his  hemiplegic  leg,  he  cannot  do  so  without  at  the  same  time  dorsi- 
flexing  the  ankle  involuntarily.  This  is  the  so-called  "  tibialis 
phenomenon  "  of  Striimpell.  Similarly  in  the  upper  limb  we  may 
note  an  analogous  "  pronation  phenomenon,"  consisting  of  a 
forced  pronation  on  attempting  to  flex  the  elbow. 

Some  cases  of  organic  hemiparesis  are  associated  with  tonic 
innervation  of  the  paresed  limbs.  ^  This  phenomenon  is  usually 
best  marked  in  the  upper  limb.  It  is  shown  by  an  inability  to 
relax  the  muscles  after  a  voluntary  movement,  exactly  similar  to 
the  tonic  spasm  of  myotonia  congenita  (see  p.  262).  The  pheno- 
menon of  tonic  innervation  disappears  if  the  paralysis  becomes 
more  profound  and  does  not  occur  in  complete  hemiplegia  :  it 
apparently  demands  a  relative  integrity  of  the  cortico-spinal  motor 
path. 

With  an  upper  neurone  lesion,  in  the  vast  majority  of  cases 
the  muscles  of  the  paralysed  limb  undergo  no  appreciable  atrophy, 
save  perhaps  to  a  very  slight  degree  from  disuse.  But  there 
are  occasional  exceptions  to  this  rule,  as  in  some  cases  of 
hemiplegia  which  are  associated  with  muscular  atrophv,  chiefly  in 
the  region  of  the  shoulder  or  in  the  intrinsic  muscles  of  the  hand. 
Such  atrophies  are  often  (but  not  always)  secondary  to  arthritic 
changes  in  the  joints.  But  however  intense  the  amyotrophy  of 
hemiplegia  may  be,  the  electrical  reactions  of  degeneration  are 
never  present.  Degenerative  reactions  (commonly  referred  to  as 
"  R.D.")  are  pathognomonic  of  a  nuclear  or  infra-nuclear  lesion. 
Not  that  R.D.  are  necessarily  present  in  every  lower  neurone 
lesion,  for  a  slight  lesion  of  a  nerve-trunk  may  produce  mascular 
palsy  without  R.D.,  and  in  many  nuclear  lesions,  for  example 
in  progressive  muscular  atrophy,  the  reactions  in  the  affected 
muscles  are  mixed,  owing  to  the  fact  that  degenerated  and 
healthy  muscle-fibres  are  intermingled  in  the  same  muscle,  the 
former  giving  R.D.,  the  latter  being  normal  in  reaction.  Again, 
in  the  motor  weakness  occurring  in  the  different  varieties  of 
myopathy,  there  is  simple  diminution  both  to  faradism  and 
galvanism,  but  no  true  R.D.,  even  in  the  most  advanced  cases. 

^  Wilson  and  Walshe,  Brain,  1914,  vol.  xxxvii.  p.  199. 


224  NERVOUS   DISEASES 

The  reflexes  in  upper  and  lower  neurone  lesions  will  be  dealt  with 
more  fully  in  a  later  chapter  (p.  330). 

With  reference  to  the  differential  diagnosis  between  an  upper 
and  a  lower  neurone  lesion,  it  will  be  observed  that  no  single  sign 
of  the  six  we  have  mentioned  is  pathognomonic,  yet  the  sum  of  the 
various  points  usually  enables  us  without  difficulty  to  settle  with 
which  of  the  two  neurones  we  have  to  deal.  Sometimes  there  is  a 
combined  lesion  of  upper  and  lower  neurones,  as  in  a  transverse 
myehtis  or  a  myelomalacia.  Here  the  phenomena  at  the  level  of 
the  lesion  will  be  of  a  flaccid,  lower  neurone  type,  due  to  destruc- 
tion of  the  anterior  cornua  and  anterior  roots,  whilst  below  that 
level  there  is  a  spastic  paraplegia  of  cortico-spinal  type,  from 
interruption  of  the  pyramidal  tracts. 

Motor  Palsies  of  Upper  Neurone  Type. — The  signs  and 
symptoms  vary  according  to  the  level  at  which  the  cortico- 
spinal tract  is  damaged.  The  following  are  the  chief  sites  at 
which  a  lesion  may  occur,  and  the  diagnostic  signs  corresponding 
to  each  (see  Fig.  6,  p.  8). 

A  cortical  lesion  in  the  pre-central  convolution  is  often 
locaHsed  to  a  single  limb  and  is  more  Ukely  to  produce  a  mono- 
plegia than  a  hemiplegia,  since  only  a  very  extensive  cortical 
lesion  would  produce  a  complete  hemiplegia,  affecting  face,  arm 
and  leg.  What  we  usually  find  is  either  a  pure  monoplegia — crural, 
brachial,  or  facio-hngual,  or,  if  the  lesion  be  somewhat  larger,  an 
associated  monoplegia — brachio-crural,  or  facio-brachial.  Cortical 
motor  paralysis  is  commonly  associated  with  local  epileptiform 
attacks  of  the  paralysed  hmb,  because  disease  may  irritate  the 
cortex  in  addition  to  paralysing  it.  The  monoplegic  limb  frequently 
shows  a  cortical  type  of  anaesthesia,  which,  as  we  have  already 
seen,  is  shght  in  degree,  more  marked  at  the  periphery  of  the 
limb,  and  often  transient  in  character. 

A  strictly  locahsed  suhcortical  lesion  is  often  indistinguishable 
from  a  cortical  one,  save  by  the  absence  of  irritative  epileptiform 
phenomena ;  and  in  many  cases  the  lesion  is  both  cortical  and 
subcortical. 

A  lesion  in  the  motor  path  at  the  level  of  the  internal  capsule, 
inasmuch  as  all  the  pjn-amidal  fibres  have  by  this  time  converged 
to  form  a  compact  strand,  produces  no  longer  a  monoplegia  but  a 
complete  hemiplegia,  affecting  face,  arm  and  leg.  There  are  no 
Jacksonian  convulsions  as  in  a  cortical  lesion.     If  the  capsular 


PARALYSIS    OF    UPPER    NEURONE    TYPE       225 

lesion  extends  backwards  from  the  motor  into  the  sensory  tract,  or 
into  the  optic  thalamus,  there  may  be  a  coexistent  hemi-ansesthesia, 
but  this  is  not  common. 

A  thalamic  lesion  is  sometimes  associated  with  hemi-athetosis 
of  the  hemiplegic  side  ;  this  athetosis  does  not  appear  immediately 
after  the  attack  of  apoplexy,  but  develops  gradually  in  the  coarse 
of  many  weeks.  A  still  more  extensive  lesion,  extending  back- 
wards along  the  capsule  from  the  motor  tract,  through  the  sensory 
path  and  into  the  optic  radiations,  will  cause  hemiplegia,  hemi- 
ansesthesia  and  hemianopia. 

In  rare  cases  we  may  have  an  ijyso-lateral  hemiplegia  in 
which,  for  example,  a  lesion  of  the  left  cerebral  hemisphere  pro- 
duces a  left-sided  hemiplegia.  Some  of  these  cases,  according  to 
Marie,  are  due  to  congenital  non-decussation  of  the  pyramids  ; 
others  result  from  a  dural  haematoma,  a  meningeal  haemorrhage 
or  a  superficially  situated  tumour,  whereby  the  contra-lateral 
pyramidal  tract  is  compressed  against  the  base  of  the  skull. 
From  the  surgical  point  of  view,  we  must  also  bear  in  mind  the 
occasional  occurrence  of  a  false  ipso-lateral  hemiplegia,  when  a 
blow  on  one  side  of  the  head,  say  the  left,  is  followed  by  a  left- 
sided  hemiplegia.  Such  cases  are  generally  due  to  injury  of  the 
opposite  {i.e.  the  right)  hemisphere  by  "  contre-coup." 

A  lesion  in  the  crus  cerebri  is  recognised  by  the  coexistence 
of  third  nerve  palsy  on  one  side,  with  hemiplegia  of  the  opposite 
face,  arm  and  leg,  usually  most  marked  in  the  face.  This  variety 
of  alternate  paralysis  is  known  as  Weber's  syndrome  (see  Fig.  94). 
The  third  nerve  palsy  is  often  incomplete.  When  the  lesion 
extends  into  the  tegmentum  and  imphcates  the  neighbourhood  of 
the  red  nucleus,  it  may  produce  a  unilateral  tremor  or  a  hemi- 
ataxy  of  the  hemiplegic  side,  combined,  as  before,  with  a  third 
nerve  affection  on  the  side  of  the  brain  lesion ;  this  combination 
is  known  as  Benedikfs  syndrome.  If  the  lesion  extends  outwards 
so  as  to  implicate  the  optic  tract  as  it  winds  round  the  outer  side 
of  the  crus,  there  may  be  superadded  a  hemianopia. 

As  we  come  downwards  along  the  pyramidal  tract  into  the 
pons  and  medulla,  the  type  of  hemiplegia  changes ;  there  is  no 
longer  third  nerve  palsy,  but  on  reaching  the  level  of  the  facial 
nerve,  another  variety  of  alternate  hemiplegia  appears.  This 
consists  of  facial  palsy,  peripheral  in  type,  on  the  side  of  the  lesion, 
together  with  hemiplegia  of  the  arm  and  leg  on  the  opposite  side, 


226 


NERVOUS    DISEASES 


the  so-called  Millard-Gubler  syndrome.  Other  cranial  nerves  on  the 
side  of  the  pontine  or  bulbar  lesion,  for  example,  the  trigeminal, 
the  sixth,  or  the  hypoglossal,  may  be  affected  together  with  the 
pyramidal  tract.  Paralysis  of  these,  as  in  the  Millard-Gubler  syn- 
drome, may  co-exist  with  hemiplegia  of  the  opposite  arm  and  leg, 
but  such  cases  are  rare.  As  they  descend  through  the  medulla  the 
pyramidal  tracts  of  opposite  sides  converge  and  eventually  lie 
so    close  together  that  at  this  level    a   strictly  unilateral   lesion 


Fig.  94. — Lesion  of  left  crus  cerebri — "  Weber's  syndrome."  Patient  is 
looking  upwards  and  attempting  to  show  the  teeth  on  both  sides. 
There  is  dilatation  of  the  left  pupil  and  paralysis  of  the  left  superior 
rectus,  together  with  hemiplegia  of  the  right  face,  arm  and  leg. 

seldom  occurs,  there  being,  as  a  rule,  damage  to  both  pyramidal 
tracts,  affecting  the  limbs  of  both  sides,  though  perhaps  in  unequal 
degree.  And  together  with  this,  there  are  "  bulbar  "  symptoms 
— disorders  of  articulation,  phonation,  or  deglutition,  from  impli- 
cation of  the  tenth,  eleventh  and  twelfth  cranial  nerves  or  nuclei. 
The  diagnosis  of  motor  paralysis  due  to  lesions  of  the  pyramidal 
tract  within  the  spinal  cord  depends  on  the  level  of  the  lesion.  The 
two  pyramidal  tracts  decussate  at  the  lower  end  of  the  medulla 
oblongata,  so  that  a  unilateral  lesion  of  the  spinal  cord  pro- 
duces an  ipso-lateral  instead  of  a  contra-lateral  motor  paralysis. 
If  the  lesion  be  in  the  cervical  region,  the  arm  and  leg  on  the 


PARALYSIS    OF    UPPER   NEURONE   TYPE        227 

corresponding  side  will  be  affected ;  but  if  it  be  situated  below 
the  cervical  enlargement,  the  leg  on  the  side  of  the  lesion  suffers 
alone.  A  primary  unilateral  lesion  of  the  cord  generally  interrupts 
not  only  motor  but  sensory  paths,  and  produces  the  well-known 
Brown-Sequard  paralysis,  to  which  reference  has  already  been  made. 

Bilateral  motor  paralysis  of  upper  neurone  type  is  due  to  bi- 
lateral lesions,  which  may  be  situated  either  in  the  brain  or  in  the 
spinal  cord.  When  both  p}Tamidal  tracts  are  affected  within  the 
brain  (and  the  commonest  cause  is  a  double  focus  of  softening,  in 
the  region  of  the  posterior  part  of  the  lenticular  nucleus,  although 
less  commonly  the  lesions  are  cortical  or  subcortical)  a  double 
hemiplegia  is  the  result.  In  these  cases  of  double-hemiplegia  or 
diplegia  there  are,  besides  the  signs  of  hemiplegia  on  both  sides 
(frequently  unequal  in  degree),  what  are  known  as  "  pseudo-bulbar  " 
phenomena.  In  pseudo-bulbar  paralysis,  the  symptoms  of  which  we 
have  already  studied  (p.  123),  it  is  uncommon  for  the  two  attacks 
of  hemiplegia  to  occur  simultaneously  on  the  two  sides  ;  they  more 
usually  occur  successively,  and  it  is  only  after  the  hemiplegia  has 
become  bilateral  that  the  pseudo-bulbar  symptoms  appear.  Such 
patients  are  generally  excessively  emotional,  tending  on  sHght 
provocation  to  laugh  or,  more  frequently,  to  weep  with  a  peculiar 
"  spastic "  wail,  and  an  unnatural  slowness  of  expressional 
movement. 

Bilateral  pyramidal  lesions  within  the  spinal  cord  produce  para- 
plegia, affecting  all  four  Kmbs  if  the  lesion  be  above  the  cervical 
enlargement,  but  affecting  the  lower  limbs  alone  if  the  lesion  be 
below  the  cervical  region ;  it  is  commonly  of  the  ordinary 
spastic  tjTpe,  with  increased  deep  reflexes.  If  the  sensory 
tracts  be  interrupted  by  the  same  lesion  as  that  which  has  affected 
the  motor  tracts,  we  have  superadded  an  anaesthesia  the  upper  Hmit 
of  which  corresponds  to  that  of  the  highest  affected  segment. 
Such  bilateral,  combined,  sensory  and  motor  paralysis  is  usually 
accompanied  by  loss  of  control  of  the  sphincters.  (So  long  as  a  spinal 
cord  lesion  remains  unilateral,  we  do  not,  as  a  rule,  have  sphincter 
trouble.)  If  the  cord  lesion  be  sufficiently  extensive  to  implicate 
the  anterior  comua,  there  wiU  be  muscular  atrophy,  locahsed  to 
the  segment  affected,  i.e.  at  the  upper  boundary  of  the  spastic 
paraplegia.  But  it  is  important  to  remember  that  if  the  lesion 
of  the  cord  be  one  which  completely  divides  it  {e.g.  a  stab  or  bullet- 
wound),  so  that  there  is  no  connection  between  the  cord-segments 


228  NERVOUS    DISEASES 

above  and  below  tbe  lesion,  the  paraplegia  is  then  flaccid  in  type 
and  the  deep  reflexes  are  absent  in  the  paralysed  limbs.  The 
plantar  reflexes,  however,  persist  and  are  of  the  extensor  type,  be 
the  lesion  complete  or  incomplete. 

The  differential  diagnosis  between  tumours  arising  within 
the  spinal  cord  and  those  growing  from  without,  is  some- 
times difficult.  In  extra-medullary  tumours,  arising  from  the 
nerve-roots  or  meninges  on  the  posterior  aspect  of  the  cord, 
root-pains,  unilateral  or  bilateral,  usually  precede  the  gradually 
progressive  signs  of  a  transverse  lesion,  more  or  less  complete,  of  the 
cord.  In  intra -medullary  tumours,  root  symptoms  are  absent,  and 
trophic  changes  in  the  joints,  bones,  and  skin  are  more  common  (see 
p.  323,  Syringomyelia).  An  extra -medullary  tumour  situated  later- 
ally sometimes  compresses  the  cord  so  as  to  produce  an  incomplete 
Brown-Sequard  syndrome. 

Thus  in  one  case  of  my  own,  in  which  an  endothelioma  was  re- 
moved from  the  first  thoracic  root  on  the  right  side,  the  patient,  in 
addition  to  root-pains  along  the  inner  border  of  the  right  upper  limb, 
had  asymmetrical  spastic  paraplegia,  more  marked  in  the  right  leg, 
together  with  impairment  of  thermal  and  pain  sense  in  the  left  leg 
and  left  side  of  the  trunk. 

But  if  the  extra-medullary  growth  starts  in  front  of  the  cord, 
root-pains  are  absent  or  late.  If  the  anterior  roots  be  involved, 
muscular  atrophy  of  root  distribution  is  a  valuable  focal  sign, 
and  owing  to  the  oblique  direction  of  the  nerve  roots,  such  radicular 
atrophy  is  only  seen  above  the  level  of  the  pyramidal  symptoms.  In 
cases  of  intra-medullary  lesion,  on  the  other  hand,  in  which  muscular 
atrophy  is  due  to  destruction  of  anterior  cornua,  the  muscular 
atrophy  corresponds  in  level  to  the  maximum  point  of  the  lesion, 
and  pyramidal  symptoms  (notably  the  reflexes  of  spinal  automatism) 
may  be  present  above  the  level  of  the  muscular  atrophy.  Spon- 
taneous reflex  spasms  of  the  lower  limbs  are  commoner  in  extra- 
medullary  than  in  intra-medullary  growths. 

The  tendency  is  to  localise  a  spinal  tumour  below  its  actual 
level.  Sometimes  valuable  indications  are  provided  by  studying 
the  vibration  sense  of  the  vertebral  spines,  for  such  sensibility  is 
often  lost  up  to  the  upper  level  of  the  growth. 

Occasionally  a  diagnosis  of  extra-medullary  tumour  is  made, 
whereas  operation  or  autopsy  shows  the  condition  to  be  one,  not  of 
tumour  but  of  circumscribed  subacute  or  chronic  lepto-meningitis. 


PARALYSIS    OF    UPPER    NEURONE    TYPE        229 

This  mistake  may  sometimes  be  avoided  by  studying  the  exact 
distribution  of  the  initial  root-pain.  In  tumour  this  pain  is 
localised  to  a  single  root  at  the  start ;  in  meningitis  the  pain  is 
more  diffuse,  affecting  a  considerable  number  of  root-areas. 

Often  the  lesion  is  not  horizontal,  but  higher  on  one  side 
than  the  other,  and  then  the  upper  limit  of  the  anajsthesia  will  be 
correspondingly  uneven  on  the  two  sides,  and  the  distribution  of 
muscular  atrophy  from  anterior  cornual  destruction  corresj)ond- 
ingly  asymmetrical. 

Another  point  which  sometimes  helps  us  to  recognise  the  upper 
limit  of  a  spinal  cord  lesion  is  by  studying  the  skin-area  of  inhibi- 
tion of  knee-  or  ankle-clonus  (see  p.  342).  To  observe  this,  we 
first  ask  a  skilled  assistant  to  eUcit  the  clonus ;  once  started,  this 
is  sustained  indefinitely,  so  long  as  the  requisite  tension  of  the 
muscles  is  maintained.  Whilst  the  clonus  is  going  on,  we  now 
energetically  stimulate  the  skin  of  the  lower  limb  or  lower  part  of 
the  trunk,  e.g.  by  pinching  ;  the  clonus  at  once  becomes  arrested. 
This  inhibition  only  occurs  on  stimulation  of  the  skin-areas  below 
the  upper  level  of  the  cord  lesion  ;  stimulation  of  the  skin  above 
the  level  of  the  lesion  produces  no  inhibition  of  clonus. 

Occasionally  a  spinal  tumour  has  a  considerable  vertical  length, 
extending  through  several  segments  of  the  spinal  cord.  The  lower 
limit  of  such  a  growth  is  more  difficult  to  determine  than  its  upper 
boundary.  We  can  sometimes  obtain  valuable  information  by  a 
study  of  certain  reflexes  of  spinal  automatism,  which  are  often 
present  in  organic  pyramidal  lesions  and  which  are  analogous  to 
phenomena  demonstrated  by  Sherrington  ^  in  the  dog  whose 
brain-stem  has  been  divided,  whether  in  the  upper  cervical  region 
(spinal  dog)  or  at  the  level  of  the  mid-brain  (decerebrate  dog)  and 
described  by  him  as  the  flexion-reflex,  crossed  extension  reflex, 
"  mark-time "  reflex,  &c.  In  the  human  subject  with  organic 
pyramidal  disease,  e.g.  in  spinal  cord  lesions,  the  most  constant 
reflex  of  spinal  automatism  is  a  movement  of  flexion  or  shortening 
of  the  lower  limb  at  all  joints,  including  flexion  of  the  hip  and 
knee,  with  dorsiflexion  of  the  ankle  and  toes,  especially  the  hallux  : 
phf^nomdne  des  raccourcisseurs.  For  this  phenomenon  Babinski  ^ 
proposed  the  attractive  title  of  "  defensive  "  reflex,  but  as  Strohl  ^ 

^  Sherrington,  Journal  of  Physiology,  1910,  xl.  p.  23. 

^  Babinski  and  Jarkowski,  Revue  neurologique,  1910,  p.  666. 

'  Strohl,  Presse  meiicale,  March  11,  1914,  p.  195. 


230  NEKVOUS  DISEASES 

has  pointed  out,  Marie's  ^  term  of  "  reflex  of  spinal  automatism  " 
is  preferable.  The  phenomenon  is  elicited  by  stimulating  the 
skin  of  the  lower  limb  or  lower  part  of  the  trunk  (by  pinching, 
pricking,  scratching,  locahsed  heat  or  cold,  faradism,  &c.)  and 
also  by  stimulation  of  deeper  structures  {e.g.  by  passive  flexion  of 
the  toes,  by  deep  painless  stroking  of  the  sole,  especially  along  its 
outer  hah,  or  by  firm  lateral  compression  of  the  foot).  The  reflex 
movement  of  the  stimulated  limb  does  not  always  "  defend  "  it 
by  withdrawing  it  from  the  stimulus ;  on  the  contrary,  it  may 
sometimes  bring  it  nearer  {e.g.  when  the  stimulus  is  at  the  back  of 
the  cah).  The  extensor  'plantar  reflex  of  pyramidal  disease  (see  p.  333) 
is  an  integral  part  of  this  larger  flexion-reflex.  Sometimes  both 
lower  Umbs,  and  not  merely  one,  become  flexed.  These  flexion 
movements  occur,  apparently  spontaneously,  in  the  well-known 
"  flexor  spasms  "  seen  in  certain  cases  of  paraplegia. 

In  cases  of  spastic  paralysis  with  extensor  rigidity,  in  addition 
to  flexion  of  the  lower  limb  thus  stimulated,  we  also  produce  a 
simultaneous  extension  of  the  opposite  lower  limb,  "  phenomdne 
(T allongement  croisd,^^  in  which  there  is  extension  of  the  hip  and 
knee,  with  plantar  flexion  of  the  ankle  and  toes.  This  phenomenon 
may  also  occur  in  hemiplegia,  on  stimulating  the  sole  of  the  non- 
paralysed  foot.^ 

The  cutaneous  area  from  which  these  reflexes  of  spinal  auto- 
matism can  be  ehcited  varies  in  extent  in  different  cases,  the  sole 
of  the  foot  being  the  most  constant  reflexogenous  area.  The 
upper  level  of  the  trunk,  up  to  which  they  can  be  evoked  by 
cutaneous  stimulation,  indicates  the  lower  level  of  the  lesion  which 
is  compressing  the  cord.  In  any  individual  case  the  skin  of  the 
trunk  should  be  explored  on  repeated  occasions,  both  from  above 
downwards  and  from  below  upwards,  noting  the  level  at  which  the 
cutaneous  reflexes  of  spinal  automatism  appear  or  disappear.  There 
is  one  particular  fallacy  which  we  must  be  careful  to  avoid,  viz. 
that  a  stimulus  above  the  level  in  question,  especially  if  it  be  a 
painful  one,  may  produce  a  voluntary  movement  of  the  upper 
part  of  the  body,  which  by  dragging  on  the  passive  lower  limbs 
may  evoke  a  false  reflex,  thus  leading  us  to  place  the  lower  level 
of  the  lesion  too  high  up. 

Intra-thecal  growths  have,  as  a  rule,  a  relatively  short  vertical 

^  Marie  and  Foix,  Semaine  medicale,  Oct.  22,  1913,  p.  505. 
2  Walshe,  Brain,  1914,  vol.  xxxvii.  pp.  269-336. 


PARALYSIS    OF    UPPER    NEURONE    TYPE         231 

extent,  and  they  rarely  compress  more  than  one  or  two  segments 
of  the  cord.  On  the  other  hand,  extra-thecal  growths,  by  the 
time  they  produce  compression  of  the  cord,  are  usually  of  consider- 
able length.  This  maxim  also  applies  to  hypertrophic  pachy- 
meningitis and  to  the  pachy-meningitis  associated  with  spinal 
caries.  Therefore,  in  a  case  of  compression  paraplegia,  in  which 
the  reflexes  of  spinal  automatism  are  well  marked  and  in  which  the 
difference  in  level  is  considerable  between  the  upper  limit  of  the 
anaesthesia  and  that  of  the  cutaneous  reflexes  of  spinal  automatism, 
we  have  probably  to  deal  with  an  extra-thecal  tumour,  or  with  a 
pachy-meningitis.  If,  on  the  other  hand,  the  two  levels  practically 
coincide,  we  incline  to  diagnose  an  intra-thecal  growth. 

We  also  meet  with  cases  of  bilateral  spastic  paraplegia  without 
any  affection  of  sensation.  Such  cases  may  be  examples  of 
slowly  progressive  primary  lateral  sclerosis,  a  rare  disease,  or  what 
is  more  usual,  of  amyotrophic  lateral  sclerosis,  in  which  the  signs  of 
a  progressive  muscular  atrophy  are  superadded  to  rigidity  of  the 
lower  Hmbs  with  increased  deep  reflexes.  A  pure  motor  paraplegia 
is  more  frequently  due  to  disseminated  sclerosis,  to  an  imper- 
fectly recovered  transverse  myelitis,  or  to  some  other  vascular 
lesion,  such  as  thrombosis  or  hemorrhage,  at  a  stage  in  which 
the  sensory  functions  have  become  restored,  whereas  the  motor 
tracts  remain  permanently  sclerosed.  The  history  of  the  case  is 
sufficient  to  distinguish  between  these  diseases. 

Syringomyeha,  when  it  affects  the  pyramidal  tracts,  may  also 
produce  a  spastic  type  of  paraplegia ;  but  it  is  readily  recognised 
by  the  characteristic  dissociated  anaesthesia,  to  which  we  have 
already  referred  (p.  211),  and  by  the  frequent  coexistence  of 
atrophic  changes  in  the  bones,  joints  and  muscles,  and  muscular 
atrophy  when  the  anterior  cornua  are  imphcated  in  the  gUomatous 
process. 


CHAPTER  XIV 

ORGANIC  MOTOR  PARALYSIS  OF  LOWER  NEURONE  TYPE 

Motor  Palsies  of  Lower  Neurone  Type. — Here,  as  in  upper 
neurone  lesions,  the  signs  and  symptoms  differ  according  to  the 
level  at  which  the  spino-muscular  neurone  is  diseased.  The  most 
important  diagnostic  fact,  for  localising  purposes,  is  the  presence 
or  absence  of  sensory  phenomena.  If,  in  a  lower  neurone  motor 
palsy,  sensory  changes  are  present,  we  have  to  do  with  a  lesion 
of  a  mixed  nerve,  that  is,  of  a  nerve  containing  sensory  as  well 
as  motor  fibres.  If,  on  the  other  hand,  sensory  changes  are  absent 
throughout  the  course  of  the  disease,  the  spino-muscular  neurone 
is  probably  affected,  either  before  it  is  joined  by  the  sensory  fibres 
{i.e.  the  lesion  is  in  the  anterior  cornu  or  anterior  nerve-root),  or 
after  it  has  parted  company  with  them  {i.e.  the  lesion  is  in  a 
purely  motor  nerve-branch  or  in  the  muscle  itself). 

A  lesion  of  the  anterior  cornu  within  the  cord  (as  of  its  homo- 
logue  in  the  motor  nuclei  of  the  bulb)  is  unassociated  with  any 
sensor}^  paralysis,  and  therefore  produces  a  pure  motor  palsy  of 
the  corresponding  muscle  fibres.  A  lesion  of  the  anterior  nerve-root, 
emerging  from  the  anterior  cornu,  produces  identical  signs,  and  is 
often  indistinguishable  from  an  intra-spinal  nuclear  lesion.  In 
nuclear  or  anterior-root  lesions,  therefore,  we  find  pure  motor  palsy, 
of  lower  neurone  type,  unassociated  with  any  sensory  change.  The 
commonest  examples  of  such  lesions  are  chronic  anterior  poHo- 
myelitis  (progressive  muscular  atrophy)  and  certain  types  of  lead 
paralysis.  Acute  anterior  polio-myelitis  (infantile  paralysis  of 
spinal  type)  in  the  early  days  or  weeks  of  the  disease  is  frequently 
associated  with  pain  and  tenderness  of  the  limbs.  As  the  malady 
subsides  into  the  chronic  stage,  the  pain  and  tenderness  pass  ofi. 
Landry's  paralysis  is  a  pm-e  motor  paralysis  of  the  whole  spino- 
muscular  neurone,  to  which  we  shall  refer  presently.  A  nuclear  or 
anterior  root  lesion  is  further  characterised  by  the  "  root "  dis- 
tribution of  the  motor  paralysis,  so  that  in  this  respect  it  differs 
from  the  paralysis  due  to  a  lesion  of  a  peripheral  nerve  (see  Tables 

232 


PARALYSIS   OF    LOWER    NEURONE    TYPE        233 


of  Root  Distribution,  p.  41).  Lesions  of  peripheral  mixed  nerves 
are  always  associated,  at  the  onset  at  least,  with  sensory  changes. 
In  the  case  of  lesions  of  peripheral  purely  motor  nerves  {e.g. 
the  nerve  of  Bell  to  the  serratus  magnus),  the  distribution  of 
the  motor  palsy  is  totally  unlike 
that  of  a  nuclear  or  anterior  root 
lesion. 

To  distinguish  between  a  nuclear 
and  an  anterior  root  lesion  is  some- 
times difficult,  and  may  in  some 
instances  be  impossible.  The  co- 
existence of  spastic  phenomena  corre- 
sponding to  lower  parts  of  the  cord 
points  to  an  intra-spinal  lesion,  and 
indicates  a  co-existing  lesion  of 
the  adjacent  pyramidal  tract.  Total 
escape  of  the  pyramidal  tract,  on  the 
other  hand,  would  suggest  an  anterior 
root  lesion,  though  not  necessarily  so, 
seeing  that  acute-anterior  polio -myelitis 
does  not  affect  the  pyramidal  tract.  An 
other  point  which  may  sometimes  help 
us  is  the  subsequent  course  of  the 
disease ;  if  the  paralysed  muscles 
recover,  this  is  in  favour  of  an  extra- 
medullary  anterior  root  lesion  rather 
than  an  affection  of  the  anterior 
cornu,  inasmuch  as  regeneration  of 
nerve-fibres  only  occurs  in  extra- 
spinal  lesions,  an  intra-spinal  lesion  of  the  grey  matter  being 
irreparable. 

A  pure  anterior  cornual  lesion,  with  its  absence  of  cutaneous 
anaesthesia,  can  only  be  confounded  with  a  lesion  either  in  a  purely 
motor  nerve,  or  with  one  in  the  muscle-fibres  themselves.  The 
history  of  the  onset  of  the  disease  is  of  great  importance,  so  also 
is  the  exact  distribution  of  the  muscular  paralysis.  The  two  chief 
diseases  specially  affecting  the  anterior  cornua  are  infantile 
paralysis  and  progressive  muscular  atrophy. 

Acute  anterior  polio-myelitis,  or  infantile  spinal  paralysis,  is  a 
constitutional  disease  due  to  an  infective  virus.     After  an  incuba- 


FiG.  95.  —  Old  acute  anterior 
polio-mj'elitis,  with  atrophy 
of  deltoid  and  biceps,  and 
deficient  growth  of  the 
humerus  on  the  left  side. 


234 


NEEVOUS   DISEASES 


tion  period  of  six  or  eight  days,  during  which  there  are  no  symptoms, 
there  is  an  acute  onset,  usually  febrile.  The  fever  reaches  its 
maximum  about  the  third  day,  and  it  is  generally  at  this  stage 
that  evidences  of  muscular  paralysis  are  made  out.  Even  before 
the  onset  of  paralysis,  the  blood  shows  a  leucocytosis,  and  if  we 
examine  the  cerebro-spinal  fluid  we  note  the  presence  of  lympho- 
cytosis and  of  globulin  (see  later,  p.  441).  The  virus,  whilst 
causing  congestion  of  various  organs,  including  the  spleen  and 

lymphatic  glands,  together  with 
multiple  necrotic  lesions  of  the 
liver,  is  neurotropic,  i.e.  it  has  a 
specially  intense  effect  upon  the 
central  nervous  system  and  its 
meninges,  and  produces  a  special 
perivascular  infiltration  around 
the  anterior  spinal  arteries,  which 
supply  the  anterior  horns.  The 
spinal  meninges  being  also 
hypersemic,  there  are  pains 
in  the  limbs,  aggravated  by 
passive  movement.  A  large  num- 
ber of  muscles,  sometimes  in 
all  four  limbs,  may  originally  be 
paralysed.  But  in  a  week  or  two 
most  of  the  paralysis  clears  up, 
leaving  a  residuum,  almost  always 
unilateral,  of  paralysed  muscles 
which  undergo  rapid  wasting. 
There  is  no  exaggeration  of  tendon  reflexes  below  the  level  of  the 
lesion,  since  the  pyramidal  tract  is  unaffected.  Eigs.  95,  96,  and 
97  are  examples  of  cases  of  old  infantile  paralysis,  showing  the 
extreme  degree  of  atrophy  which  results,  and  if  the  disease  occurs 
in  childhood,  as  is  most  often  the  case,  the  subsequent  want  of 
growth  in  the  limb.  The  wasted  limb  is  often  cold  and  blue, 
and  the  patient  can  frequently  tolerate,  without  pain,  faradic 
stimulation  of  a  strength  which  is  intolerable  in  the  sound  limbs. 

Chronic  anterior  polio-myelitis,  or  progressive  muscular 
atrophy,  has  a  gradual,  insidious  onset.  It  occurs  almost  always 
in  adults  and,  though  beginning  unilaterally,  generally  becomes 
bilateral.     It    usually   shows    itself    first   in   the    small    intrinsic 


Fig.  96. — Old  infantile  paralysis  with 
total  loss  of  deltoid  and  biceps. 
Shows  action  of  the  supinator 
longus   in  flexion  of  elbow. 


PARALYSIS   OF    LOWER    NEURONE    TYPE         235 


muscles  of  tlie  hands  (Aran-Duchenne  type,  see  Fig.  98) ;  more 
rarely  it  begins  in  the  shoulder  muscles.  In  this  disease  we  observe 
fibrillary  worm-like  tremors  in  the  wasting  muscles,  with  electrical 
reactions  which  are  a  mixture  of  R.D.  with  healthy  reactions. 
This  is  because  here  and  there  in  the  diseased  area  a  healthy  an- 
terior oornual  cell  survives,  together  with  its  corresponding  healthy 


Fig.    97. — Old    infantile    paralysis    (acute 
-  anterior  polio-myelitis).    Paralysis  and  at- 
rophy of  all  the  muscles  below  the  elbow, 
with  exception  of  supinator  longus. 


Fig.  98. — Progressive  mus- 
cular atrophy  in  a  man 
aged  32.  The  patient  was 
also  tabetic. 


muscle^fibre.  If  the  adjacent  pyramidal  tracts  be  sclerosed,  we 
have  amyotrophic  lateral  sclerosis,  in  which  the  deep  reflexes  are 
exaggerated  and  the  plantar  reflexes  extensor  in  type. 

i  Neither  in  chronic  anterior  poho-myelitis  nor  in  amyotrophic 
lateral  sclerosis  do  we  meet  with  any  sensory  changes.  Sensibility 
to  pain  and  to  temperature  should  always  be  carefully  tested  in 
such  cases,  so  as  not  to  overlook  the  early  stage  of  a  syringo- 
myelia in  which  the  ghomatous  affection  tends  to  impHcate  not 
only  the  posterior  but  also  the  anterior  cornua. 

There    is    a  rare    infantile    variety    of    progressive    muscular 


236 


NERVOUS    DISEASES 


atrophy — Werdnig- Hoffmann  type — due  to  degeneration  of  the 
anterior  cornua.  The  disease  begins  in  infancy,  often  during 
the  first  few  months  after  birth.  The  muscles  of  the  lower 
limbs  are  first  attacked,  and  exhibit  weakness  and  wasting, 
though    the  atrophy  may  be  masked  by  subcutaneous  fat.     The 


riG.  99. 


Fig.  99A. 


Figs.  99  and  99a. — -Peroneal  type  of  muscular  atrophy  (Charcot-Marie- 
Tooth).  In  spite  of  total  paralysis  below  the  knees,  the  patient  is 
still  alDle  to  stand  and  walk. 


knee-jerks  disappear  and  the  atrophied  muscles  lose  their  elec- 
trical excitability.  This  disease,  which  may  affect  several  members 
of  a  family,  gradually  spreads  upwards  to  the  medulla  and  is 
fatal,  with  bulbar  symptoms,  in  from  one  to  six  years. 

There  is  another  peculiar  form  of  muscular  atrophy  which  is 
hereditary  and  runs  in  families,  known  from  its  distribution  as 
Tooth's  "  peroneal  "  type,  or  as  the  progressive  neuritic  amyotrophy 
of  Charcot  and  Marie.     It  comes  on  in  childhood,  commencing  in 


PARALYSIS    OF    LOWER    NEURONE    TYPE 


237 


the  distal  muscles  of  the  limbs,  more  often  the  lower  limbs  and 
the  peroneal  muscles,  and  gradually  producing  weakness  with  con- 
tractures. Talipes  equino-varus  appears,  for  which  tenotomy  is 
often  done,  as  was  the  case  in  the  patient  shown  in  Fig.  99. 
But  if  the  patient's  feet  be  passively  supported,  say  by  metal 
supports  at  the  ankles,  until  the  para- 
lysis of  the  limbs  has  become  complete 
(as  in  the  patient  shown  in  Fig.  100), 
talipes  does  not  appear  even  in  the 
totally  paralysed  limb.  Later,  the 
intrinsic  muscles  of  the  hands  undergo 
wasting  (Fig.  100).  In  fact,  early 
claw-foot  and  claw-hand  in  young 
people  are  almost  pathognomonic. 
(The  only  other  disease  of  diagnostic 
importance  in  this  connection  is  pro- 
gressive hypertrophic  neuritis.)  The 
disease  hardly  ever  extends  to  the 
muscles  of  the  hips  or  shoulders.  The 
facial  and  trunk  muscles  also  escape. 
It  is  interesting  to  note  that  when  all 
the  muscles  below  the  knees  are  para- 
lysed, the  patient  may  stiU  be  able 
to  walk  alone,  although  the  gait  is 
high-stepping  from  drop-foot.  This 
was  so  in  both  the  patients  here 
figured.  The  deep  reflexes  are  lost 
in  the  atrophied  muscles.  Thus  in 
the  little  boy  (Fig.  99)  the  ankle-jerks 
were  lost,  whereas  the  knee-jerks  re- 
mained brisk,  since  the  thigh  muscles 
were  unaffected ;  in  the  girl  (Fig.  100) 
the  knee-jerks  and  ankle-jerks  were 
both  lost.     Pathologically  the  disease 

is  associated  with  atrophy  of  the  anterior  cornual  cells,  whilst 
the  anterior  nerve-roots  are  said  to  be  healthy.-^  But  there  is 
marked  degeneration  in  the  intra-muscular  nerve-fibres  of  the 
affected  muscles.  There  is  also  a  curious  degeneration  in  the 
posterior  columns,  closely  resembhng  that  of  tabes  dorsalis. 

^  Dejerine  and  Armand-Delille,  Revue  neurologique,  1903,  p.  1198. 


Fig.  100. — Peroneal  type  of 
muscular  atrophy  (Charcot- 
Marie  -  Tooth).  Showing 
atrophy  of  intrinsic  muscles 
of  hands. 


238 


NERVOUS    DISEASES 


Progressive  hypertrophic,  neuritis  is  another  family  disease 
which    begins    in    childhood    or    adolescence.      In    this    disease, 

besides  a  flaccid  muscular  atrophy 
of  the  limbs,  commencing  peri- 
pherally and  less  intense  in  the 
proximal  muscles,  and  tending  to 
produce  pes  cavus  and  claw-hand, 
there  are  marked  sensory  changes, 
resembling  those  of  tabes,  i.e. 
shooting  pains,  anaesthesia,  anal- 
gesia (especially  at  the  periphery 
of  the  limb),  loss  of  joint-sense, 
&c.  There  is  marked  ataxia  of 
the  limbs  together  with  loss  of 
the  deep  reflexes,  kypho- scoliosis, 
and  Argyll-Robertson  pupils.  In 
some  cases  exophthalmos  has  been 
observed.  1  Pathologically  we  find 
a  sclerotic  thickening  of  the  peri- 
pheral nerve-trunks,  extreme  in 
degree,  often  palpable  during  life, 
or  even  -s'isible  if  the  patient  be 
thin.  There  is  also  a  degenera- 
tion of  the  posterior  columns, 
somewhat  like  that  of  tabes  dor- 
salis.  The  muscles  show  atrophy, 
Fig.  101.— Case  of  rupture  of  C5  root  proliferation  of  sarcolemma  nuclei, 
in  a  sailor  aged  29.  There  are  ^^^  f^^^-  infiltration. 
atrophy  and  paralysis  01  deltoid,  -^ 

supra- and  infra-spinatus,  biceps,  A      lesion      of      a     Spinal    netve 

brachialis   anticus,   and  supina-       r,  ,i         nriinn     of    its     anterior 

tores  longus  and  brevis,  to-  ^\^®^  _  ^^®  ^'^^'^^  ^^  ^^^  anterior 
gether  with  anfesthesia  along  the  with  its  posterior  root,  but  above 
outer  side  of  the  limb,  from  the    ,•,  •    -         1,  -j.     j-    ;j„„     ^v,^-^ 

neck  to  the  thumb  and  index  (in  the   pomt    where  it    divides    into 

the  area  indicated  by  black  line),  branches  to  form  pleXUSes  or  in- 
The  figure  shows  the  atrophy  of     , .    .  ,      ,  .         ■,  ,      •      -, 

the  deltoid  with  downward  dis-  dividual  nerves,  IS  characterised 
placement  of  the  limb  at  the  by  ^  combination  of  motor  and 
shoulder-joint.  ,      .       ^,        t   .    -i     ,- 

sensory  paralysis,  the  distribution 
of  which  is  not  according  to  peripheral  nerves,  but  according  to 
root  areas,  motor  and  sensory  (see  Tables  of  Muscular  Localis- 
ation, p.  41,  also  Fig.  25,  p.   42).     Thus,  for  example.  Fig.    101 

'  Boveri,  La  semaine  medicale,  30th  March  1910,  p.  14.5. 


PARALYSIS    OF    LOWER    NEURONE    TYPE 


239 


is  the  photograph  of  a  sailor  wlio  received  a  violent  blow  on 
the  right  side  of  his  neck  from  an  iron  winch.  This  pro- 
duced paralysis  of  the  deltoid,  supra-  and  infra-spinatus, 
biceps,  brachialis  anticus,  and  supinatores  longus  and  brevis, 
together  with  an  area  of  cutaneous  anaisthesia  along  the 
outer  side  of  the  whole  upper  limb,  from  the  shoulder  to 
the  hand.  All  this  would  be  difficult  of  explanation  on  the 
theory   of    multiple  injuries  to    the    numerous    peripheral   nerves 


Fig.  102.  Fig.  102a. 

Figs.  102  and  102a. — Left-sided  ulnar  paralysis,  from  a  bullet-injury 
of  the  nerve  behind  the  internal  condyle  of  the  humerus.  The  area 
within  the  black  line  is  anaesthetic. 


which  supply  these  various  parts.  But  the  motor  distribu- 
tion is  that  of  the  fifth  cervical  root,  whilst  the  anaesthesia 
of  the  hand  corresponds  to  the  fifth  and  a  small  part  of  the 
sixth  root,  and  as  a  matter  of  fact  this  lesion  was  subsequently 
verified  by  operation. 

Lesions  of  peripheral  mixed  nerves,  when  complete,  are  usually 
easy  of  diagnosis,  inasmuch  as  there  are  paralysis  and  atrophy  of 
all  the  muscles  suppHed  by  the  particular  nerve,  together  with 
antesthesia  in  the  area  of  its  cutaneous  distribution.  It  is  un- 
necessary to   discuss   the   signs    of    paralysis   of   all   the    various 


240 


NERVOUS    DISEASES 


mixed  nerves.  The  question  is  one  of  anatomy.  Let  us 
select  one  or  two  illustrative  examples.  Ulnar  paralysis  affects 
certain  muscles  of  the  hand  and  forearm,  of  which  the  most 
important  diagnostically  are  the  interossei  and  the  two  ulnar 
lumbricales.  Owing  to  paralysis  of  the  interossei,  extension  of 
the  interphalangeal  joints  is  impaired,  especially  in  the  two 
ulnar    fingers    whose  lumbricales    are   also  affected.     Anaesthesia 


Fig.  103. — Paralysis  of  left  anterior  crural  nerve  from  spontaneous 
haemorrhage  in  a  case  of  hsemophilia,  showing  atrophy  and  paralysis 
of  quadriceps  extensor.  The  black  line  indicates  the  limit  of  the 
anaesthesia  on  the  outer  aspect  of  the  limb.  On  the  inner  side  of  the 
limb  it  extended  down  to  the  internal  malleolus. 


of  one  and  a  half  fingers  and  of  the  corresponding  part  of  the 
hand  is  also  present  (see  Figs.  102  and  102a).  In  old-standing 
cases,  the  unopposed  common  extensor  of  the  fingers  under- 
goes contracture  and  produces  a  claw-hand,  this  for  the  same 
reason  being  most  evident  in  the  two  ulnar  fingers.  The 
hypothenar  eminence  also  becomes  flattened  and  the  palm 
hollowed,  so  that  the  flexor  tendons  become  visible  beneath 
the  skin. 

Paralysis  of  the  anterior  crural  nerve  is  a  much  rarer  affection 
(see  Fig.   103).     From  paralysis  of  the  quadriceps  extensor  the 


PARALYSIS    OF    LOWER    NEURONE    TYPE        241 

patient  is  unable  to  extend  the  knee  on  the  affected  side  and  the 
quadriceps  undergoes  atrophy.     In  standing  erect  and  in  walking 


.  a 

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bp 


the  knee  tends  to  give  way,  and  the  patient  is  liable  to  trip  over 
small  objects.  There  is  special  difficulty  in  going  up  and  down 
stairs,  the  patient  taking  two  strides  to  each  step,  instead  of  the 

Q 


242  NERVOUS    DISEASES 

normal  alternate  movement  of  each  leg.  When  going  upstairs  lie 
leads  ofi  with  the  sound  leg  and  drags  the  paralysed  leg  np  to  the 
same  level :  when  going  downstairs  he  leads  ofi  with  the  paralysed 
leg.  From  affection  of  the  middle  and  internal  cutaneous  nerves 
and  of  the  long  saphenous  nerve,  there  is  anaesthesia  of  the  front 
of  the  thigh  and  knee  and  of  the  inner  side  of  the  leg  as  far  as  the 
ankle. 

Figs.  104  and  104a  are  from  a  case  of  division  of  the  sciatic 
nerve  from  a  bullet-wound  in  the  thigh  in  a  young  soldier.  It 
shows  how  all  the  muscles  below  the  knee  are  atrophied  and 
paralysed,  the  hamstring  muscles  having  escaped,  since  the  nerve 
was  divided  below  the  level  of  the  hamstring  branches.  Besides 
the  muscular  atrophy  with  the  usual  drop-foot,  we  have  anaes- 
thesia in  the  areas  of  the  peroneal,  musculo-cutaneous,  anterior 
tibial,  short  saphenous  and  both  plantar  nerves. 

As  a  mixed  nerve  recovers,  sensation  returns  more  rapidly 
than  motor  power,  and  protopathic  sensation  earlier  than  epicritic. 
We  must  therefore  be  prepared  to  find  that  in  a  long-standing 
case  the  sensory  loss  is  less  complete  than  in  a  recent  one, 
or  it  may  happen  that  sensation  is  quite  restored  when  motor 
power  has  not  yet  returned.  This  rule,  however,  is  by  no  means 
invariable. 

As  an  example  of  paralysis  of  a  purely  motor  nerve,  we  may 
select  the  posterior  thoracic,  or  nerve  of  Bell,  which  supplies  the 
serratus  magnus.  Fig.  105  is  from  such  a  case,  and  it  shows  the 
characteristic  "  winging  "  of  the  scapula  when  the  patient  holds 
his  arms  horizontally  forwards. 

When  a  purely  motor  paralysis  of  lower  motor  neurone  type 
is  recovered  from,  tliis  indicates  that  it  must  have  been  of  extra- 
medullary  origin,  since  regeneration  of  nerve-fibres  does  not  occur 
within  the  central  nervous  system. 

Besides  such  lesions  of  individual  nerve-trunks,  we  have  also 
to  bear  in  mind  so-called  multiple  or  peripheral  neuritis — a  very 
common  disease,  affecting  the  mixed  nerves  symmetrically  on 
both  sides,  sometimes  in  the  arms,  sometimes  in  the  legs,  some- 
times in  all  four  hmbs,  and  even  other  nerves  also  such  as  those  of 
the  soft  palate,  diaphragm,  and  so  on.  Such  neuritis,  when  affecting 
mixed  nerves,  is  easy  of  diagnosis.  The  distribution  of  the  sensory 
and  motor  abnormalities  is  characteristic.  The  patient  has  subjec- 
tive tingUng  feehngs  in  the  hands  and  feet,  and  on  examination  we 


PARALYSIS  OF  LOWER  NEURONE  TYPE   243 

find  diminution  of  sensation  to  light  touches  in  the  "  stocking  " 
and  "  glove  "  areas  of  the  limbs,  often  with  extreme  hyperajsthesia 
of  the  soles  to  pressure.  Moreover,  the  muscles  of  the  hmbs  are 
exquisitely  tender  on  being  grasped.  The  motor  paralysis,  of  the 
lower  motor  neurone  type,  specially  affects  the  anterior  tibial  and 
peroneal  groups  in  the  legs,  producing  drop-foot,  and  the  extensors 
of  the  wrists  and  fingers,  producing  drop- wrist  (Fig.  106).  The 
commonest  causes  of  multiple  neuritis  are  chronic  poisoning   by 


/ 


%* 


Fig.  105. — Paralysis  of  serratus  magnus  on  right  side.  The  patient  is 
holding  both  arms  horizontally  forwards.  The  lower  fibres  of  the 
trapezius  are  also  paralysed. 

alcohol  (commonly  associated  with  a  rapid  pulse),  arsenic  (specially 
associated  with  cutaneous  eruptions),  the  diphtheritic  poison 
(specially  associated  with  paralysis  of  the  muscles  of  accommoda- 
tion and  with  weakness  of  the  soft  palate),  beri-beri  (associated 
with  oedema  of  the  limbs  and  of  certain  serous  cavities),  diabetes, 
septicsemia,  and  other  poisons  such  as  bisulphide  of  carbon  (in 
rubber-factory  employes),  carbonic  oxide,  and  lead.  Lead  neuritis 
is  a  peculiar  form  which  practically  never  attacks  the  sensory 
fibres.  The  upper  limbs  are  usually  affected,  the  muscles  attacked 
being  the  extensors  of  the  fingers  and  wrists,  producing  wrist- 
drop.    The  long  extensors  of  the  thumb  become  paralysed  later, 


244  NERVOUS    DISEASES 

the  extensor  ossis  metacarpi  poUicis  remaining  unaffected.  The 
supinator  longus  usually  escapes,  so  that  the  disease  contrasts 
with  musculo-spiral  paralysis,  with  which  it  might  be  confused  on 
superficial  examination.  The  blue  hne  on  the  gums  and  other 
signs  of  plumbism  also  aid  us  in  the  diagnosis. 

Sometimes  the  lower  motor  neurones  are  paralysed  in  their 
entire  extent,  from  anterior  cornu  to  periphery,  the  disease  com- 
mencing in  the  motor  neurones  of  the  lowest  spinal  segments  and 


Fig.  106. — Alcoholic  neuritis  with  drop-wrist. 

spreading  upwards  towards  the  bulbar  motor  neurones.  This 
affection,  known  as  acute  ascending  faralysis,  or  Landri/s  paralysis, 
might  be  confounded  with  an  ordinary  peripheral  neuritis  were  it 
not  for  the  absence  of  sensory  changes.  The  paralysis,  com- 
mencing in  the  legs,  and  spreading  up  the  trunk  to  the  arms, 
is  of  the  usual  flaccid  type  with  loss  of  reflexes.  There  is  no 
time  for  muscular  atrophy  or  reactions  of  degeneration  to  develop, 
and  if  the  respiratory  muscles  become  paralysed  the  patient  dies, 
generally  within  a  week  from  the  onset.  The  sphincters  remain 
unaffected.  Various  organisms  have  been  cultivated  from  the 
cerebro-spinal  fluid  and  from  the  peri-dural  tissues  in  such  cases. 
The  spleen  is  frequently  enlarged,  as  in  certain  other  infective 
disorders. 

Before  leaving  the  subject  of  nerve  lesions   of  lower  motor 
neurone    type,    we    must   refer   to   lesions    of   the  cauda  equina, 


PARALYSIS    OF    LOWER    NEURONE    TYPE         245 

that  mass  of  nerve-roots,  lumbar,  sacral  and  coccygeal,  contained 
within  the  lowest  pait  of  the  spinal  theca.  According  to  the 
roots  affected,  anterior  or  posterior,  we  have  motor  and  sensory 
symptoms,  both  distributed  in  "  root "  fashion,  not  according  to 
peripheral  nerves.  The  clinical  picture  varies  according  to  the 
level  of  the  lesion.     When  the  whole  cauda  is  involved,   we  find 


Fig.  107a. 


Figs.  107  and  107a. — Paralysis  of  cauda  equina  from  Sg  roots  down- 
wards, in  a  miner  ;  due  to  vertebral  injury  from  a  fall  of  earth. 


paralysis  (of  lower  motor  neurone  type)  of  all  the  muscles  of  the 
lower  limbs,  together  with  anaesthesia  below  the  folds  of  the  groins 
in  front,  including  the  genitals,  and  below  the  upper  part  of  the 
buttocks  behind,  together  with  loss  of  control  of  the  bladder  and 
rectum.  If  the  first,  second,  and  third  lumbar  roots  escape,  the 
ansesthesia  is  less  extensive  (Fig.  25,  p.  42),  sparing  the  upper 
part  of  the  thighs.  If  the  third  lumbar  roots  escape,  thereby 
sparing  the  quadriceps,  the  motor  paralysis  is  correspondingly  less, 


246 


NERVOUS    DISEASES 


and  the  knee-jerks  survive,  thougli  there  is  still  paralysis  of  the 
glutei  and  hamstrings  and  of  all  the  muscles  below  the  knees,  with 
loss  of  ankle-jerks  and  paralysis  of  bladder  and  rectum  as  before. 

If  the  lesion  be  lower  still,  the 
area  of  paralysis,  motor  and 
sensory,  is  correspondingly 
diminished.  Below  the  second 
sacral  roots  there  is  no  para- 
lysis of  the  lower  limbs, 
but  there  is  a  characteristic 
"  saddle-shaped "  area  of 
anaesthesia  on  the  buttocks, 
perineum,  scrotum  and  penis, 
with  a  small  strip  running 
from  the  perineum  down  the 
postero-internal  aspect  of  the 
thighs.  Here  also  the  bladder 
and  rectum  are  uncontrolled, 
and  the  anal  reflexes  are  lost, 
but  there  is  no  motor  weak- 
ness of  the  lower  limbs,  and 
all  the  reflexes  of  the  lower 
limbs  are  normal.  And  so 
on,  the  area  of  paralysis  dimin- 
ishing as  we  descend,  until 
when  there  is  a  lesion  of  the 
fourth  and  fifth  sacral  and  the 
coccygeal  roots,  the  only  signs 
are  paralysis  of  the  levator 
ani,  with  anaesthesia  of  the 
anus  and  perineum,  the  sphinc- 
ter ani  remaining  intact. 

The  chief  difficulty  in  the 
diagnosis  of  lesions  in  this 
region  is  to  distinguish  be- 
tween a  lesion  of  the  cauda 
and  one  of  the  conus  medullaris — that  part  of  the  spinal  cord 
which  extends  below  the  third  sacral  segment.  In  both  cases 
the  motor  power  of  the  legs  is  unaffected,  and  there  is  anaesthesia 
of  the  "  saddle  "  area,  with  loss  of  sexual  power  and  of  control 


Fig.  108. — Bullet  wound  of  cauda  equina 
at  level  of  Sg  root  on  the  right  side 
and  S3  on  the  left.  The  genitals 
were  also  anaesthetic  with  incontin- 
ence of  both  sphincters.  There  was 
no  motor  paralysis  of  the  lower 
limbs.  The  pencil-point  indicates 
the  entrance  wound  on  the  right 
side :  the  exit  wound  is  visible  on 
the  left  side,  at  a  similar  level,  im- 
mediately above  the  iliac  crest. 


PARALYSIS    OF    LOWER    NEURONE    TYPE       247 

of  bladder  and  rectum.  Cauda  lesions,  however,  are  more  often 
gradual  in  onset  than  conus  affections,  and  are  usually  accom- 
panied by  intense  sacral  "  root  "  pains,  and  the  ultimate  anaesthesia 
of  a  Cauda  affection  is  frequently  preceded  by  cutaneous  hyper- 
sesthesia.  In  some  cauda  lesions  the  patient  suffers  from  intense 
burning  pains  in  the  perineum  and  rectum,  occurring  only  when 
in  the  sitting  posture  and  entirely  absent  when  standing,  walking, 
or  lying  down.^  This  pain  is  probably  due  to  dragging  on  the 
sacral  roots.  A  bed-sore  is  commoner  in  a  medullary  lesion  than 
in  a  Cauda  lesion.  Finally  any  "  dissociation "  of  anaesthesia, 
such  as  analgesia  or  therm-anaesthesia  without  tactile  anaesthesia, 
points  to  a  medullary  lesion.  If  both  cauda  and  conus  are  included 
in  the  same  disease,  the  cauda  symptoms  mask  the  others. 

Let  us  now  turn  to  motor  palsies  resulting  from  affections  within 
the  muscles  themselves.  Some  of  these  are  really  the  efiect  of 
diseases  of  the  intra-muscular  fibrous  tissue.  This  is  the  case  in 
acute  myositis,  in  which  disease  there  is  an  interstitial  inflammation 
within  the  muscle,  often  with  a  good  deal  of  effusion,  so  that 
any  sudden  movement  causes  acute  pain  ;  tenderness  on  pressure 
is  also  present.  Lumbago  and  the  familiar  "  stiff  neck "  are 
common  varieties,  and  their  diagnosis  usually  presents  no  diffi- 
culty. Trichiniasis  is  a  disease  in  which  the  muscle-fibres  are 
invaded  by  the  trichina  spiralis  worm.  Here  there  is  a  history 
of  the  patient  having  eaten  some  meat,  usually  pork,  which  turns 
out  to  have  been  trichinosed.  Within  a  day  or  two  he  develops 
gastro-intestinal  symptoms  and  becomes  feverish,  with  widespread 
muscular  pains,  rigidity,  and  stiffness,  especially  in  the  muscles 
of  the  limbs.  In  severe  cases  the  pharjmix,  tongue,  diaphragm, 
and  even  the  laryngeal  muscles  may  become  affected.  Together 
with  this,  there  is  a  peculiar  oedema  of  the  face  and  eyelids,  spread- 
ing thence  to  the  limbs,  and  sometimes  to  the  serous  cavities.  The 
blood  contains  a  marked  excess  of  eosinophile  leucocytes,  and  the 
temperature  is  raised.  The  symptoms  last  usually  four  or  five 
weeks. 

Sometimes,  when  a  patient  has  had  his  forearm  fractured  and 
put  up  in  splints,  the  bandages  may  be  applied  too  tightly  and 
the  blood-supply  of  the  muscles  is  interfered  with  by  the  pressure. 
As  a  result  there  are  swelUng  and  pain  in  the  hand,  and  unless 
the  bandages  be  loosened,  ischaemic  paralysis  (v.  Volkmann)  may 

1  Schlesinger,  Neurolog.  Gentralblatt,  1915,  p  450. 


248 


NERVOUS    DISEASES 


develop.  This  is  a  variety  of  myositis  following  a  partial  coagula- 
tion-necrosis, and  confined  to  the  muscles  on  the  flexor  aspect  of 
the  forearm.  At  first  the  affected  muscles  of  the  forearm  swell 
from  oedematous  effusion  ;  later  they  become  shrunken,  hard,  and 
contractured  by  zones  of  interstitial  fibrous  tissue,  with  interven- 
ing surviving  areas  of  muscle-fibres,  the  interphalangeal  and  wrist- 
joints  being  in  a  flexed  position  and  the  metacarpo-phalangeal 
joints  extended  (see  Fig.  109).  The  thumb,  which  has  a  long 
flexor  of  its  own,  often  escapes.  Active  movements  are  diminished 
or  lost,  and  passive  extension  of  the  fingers  or  wrist  is  impossible. 
The  hardness  and  stiffness  of  the  muscles  and  the  absence  of  R.D. 


Fig.  109. — Ischsemic  myositis. 

(since  the  surviving  fibres  of  the  affected  muscles  react  normally), 
together  with  the  normal  condition  of  sensation,  suffice,  with  the 
history  of  the  case,  to  distinguish  it  from  a  neuritis. 

But  we  also  meet  with  cases  of  muscular  weakness  and  atrophy 
localised  to  certain  muscles,  where  the  motor  nerves  and  nuclei 
are  healthy,  but  the  muscle  fibres  themselves  are  primarily  diseased. 
This  group  of  diseases  is  called  muscular  dystrophy,  idiopathic 
muscular  atrophy,  or  myopathy. 

CHnically  we  recognise  two  main  classes  of  myopathy  : — (1)  those 
cases  in  which  all  the  affected  muscles  waste  from  the  outset ; 
and  (2)  those  in  which  certain  muscles  undergo  a  false  enlarge- 
ment before  they  ultimately  become  smaller — so-called  pseudo- 
h5^ertrophic  paralysis.  But  there  is  really  no  essential  difference 
between  these  two  varieties.     Even  in  pseudo-hypertrophic  cases. 


PARALYSIS    OF    LOWER    NEURONE    TYPE         249 

certain  muscles  undergo  atrophy  from  the  beginning,  whilst  in 
the  others  atrophy  and  enlargement  may  be  combined  in  varying 
proportions. 

Muscular  dystrophy  is  a  congenital  disease.  Not  that  the 
symptoms  appear  at  birth,  for  the  child  is  usually  born  apparently 
healthy.  The  age  of  onset  of  noticeable  symptoms  varies  from 
two  to  sixty  years,  though  most  cases  occur  in  childhood  or  youth. 

The  chief  distinguishing  features  between  myopathic  atrophies 


Fig.  110. — Family  of  pseudo-hypertrophic  brothers,  ajt.  4,  8,  and  12. 
The  youngest  and  the  oldest  can  still  stand  and  walk  ;  the  middle 
child  can  no  longer  do  so.  In  the  two  older  boys  the  lower  fibres 
of  the  pectoral  muscles  are  absent. 

and  muscular  atrophies  of  nuclear  origin,  spinal  or  bulbar,  are  as 
follows  : — The  age  of  onset  is  earher,  as  a  rule,  in  myopathy  than 
in  progressive  muscular  atrophy  or  amyotrophic  lateral  sclerosis. 
Myopathy  often  runs  in  families  ;  progressive  muscular  atrophy  does 
not.  The  muscles  affected  are  different  in  the  two  cases.  In  pro- 
gressive muscular  atrophy  and  amyotrophic  lateral  sclerosis,  the 
wasting  most  commonly  begins  in  the  small  nmscles  of  the  hands, 
attacking  muscle-groups  corresponding  to  segments  of  the  cord.  In 
myopathy  the  larger  muscles  are  generally  affected,  whilst  the 
small  muscles  of  the  hands  escape.     Amyotrophic  lateral  sclerosis 


250  NERVOUS    DISEASES 

tends  to  spread  up  to  the  bulbar  nuclei,  and  to  produce  bulbar 
paralysis.  Myopathy  does  not  cause  bulbar  palsy.  It  is  true 
that  in  one  type  of  myopathy — the  Landouzy-Dejerine — ^the  face 
is  affected,  and  that  in  pseudo-hypertrophic  cases  the  masseters 
are  sometimes  enlarged:  but  myopathic  palsy  hardly  ever  affects 
the  tongue,  and  never  the  larynx.  In  myopathy  some  of  the 
diseased  muscles  may  be  enlarged,  whilst  others  are  wasted.  En- 
largement of   muscles  never  occurs  in  nuclear  disease.     When  a 


Fig.  111. — Pseudo-hj'pertrophic  myopathy.     Front  view, 
showing  enlargement  of  calves  and  thighs. 

myopathic  muscle  voluntarily  contracts,  we  may  sometimes  notice 
a  ball -shaped  swelling  in  the  middle  of  the  muscle,  especially 
in  the  deltoid  or  quadriceps,^  which  is  due  to  the  fact  that  the 
dystrophy  is  most  marked  at  the  extremities  of  the  muscles. 
The  long  bones  of  the  limbs  corresponding  to  the  myopathic 
muscles  undergo  a  degree  of  rarefaction  and  atrophy,  and  the 
normal  ridges  for  muscular  attachments  become  smoothed  down.^ 
Fibrillary  tremors,  which  are  so  common  in  progressive  muscular 
atrophy,  are  rare  in  myopathy.  Lastly,  in  myopathy,  unlike 
amyotrophic  lateral  sclerosis,  the  deep  reflexes  are  never  increased. 

r"  1  Merle  and  Raulot-Lapointe,  Nouvelle  Iconographie  de  la  Salpetriire,  1909, 
No.  3. 


PARALYSIS    OF    LOWER    NEURONE    TYPE         251 

In  fact,  in  myopathy  the  knee-jerk  may  disappear  from  wasting 
of  the  quadriceps. 


Fig.  112. — Pseado-hypertrophic  myopathy.     Side  view,  showing 
absence  of  lordosis  in  sitting  posture. 

The  pseudo-hypertrophic  variet}^  of  myopathy  generally  begins 
in  childhood.    It  is  the  most  rapidly  progressive  form  of  myopathy, 


FlGr.  113. — Pseudo-hypertrophic  myopathy.     Showing  method  of 
attaining  the  erect  attitude. 

and  in  most  cases  the  patient  dies  before  attaining  adult  age.  Boys 
are  affected  four  or  five  times  as  often  as  girls.  The  cases  tend  to 
run  in  families,  and  to  select  patients  of  the  same  sex  in  each  family. 


252  NERVOUS    DISEASES 

Thus  we  often  find  several  brothers  affected  whilst  the  sisters  escape. 
But  though  the  females  generally  escape  themselves,  they  tend  to 
transmit  the  disease  to  their  male  offspring,  so  that  antecedent 
cases  in  a  family  are  always  on  the  mother's  side.  Children  of 
the  same  woman  by  different  husbands  may  suffer  from  the 
disease.  It  is  therefore  unwise  to  marry  a  widow,  however  young 
and  charming,  who  has  a  pseudo-hypertrophic  child.  The  symptoms 
of  pseudo-hypertrophic  paralysis  are  entirely  motor.  The  first 
symptom  which  is  usually  noticed  is  that  the  child  falls  easily,  gets 


Fig.  114. — Pseudo-hypertrophic  myopathy.     Side  view,  showing 
lordosis  when  standing. 

up  with  difficulty,  and  cannot  run  or  jump  hke  other  children,  nor 
can  he  walk  on  his  heels,  keeping  the  feet  raised  in  front.  This  weak- 
ness gradually  increases  until  in  a  few  years  the  patient  becomes 
unable  to  stand  or  even  to  sit  up  in  bed.  The  arms  become  weak 
later  than  the  legs.  Figs.  Ill  to  114  show  two  such  patients.  In 
them  we  notice  the  characteristic  "  pot-belly  "  and  the  lordosis  when 
standing.  The  gait  is  wide-based  and  waddhng,  somewhat  hke  that 
of  the  comic-opera  sailor,  and  there  is  often  a  high-stepping  action 
to  clear  the  toes  from  the  ground.  But  most  characteristic  of  all 
is  the  way  in  which  the  patient  rises  from  the  floor  when  placed 
flat  on  his  back.  He  first  rolls  round  and  gets  on  to  his  hands  and 
knees.     Then,  keeping  his  feet  wide  apart,  he  drags  his  hands  along 


PARALYSIS   OF    LOWER    NEURONE    TYPE        253 

the  floor  towards  his  feet  until  the  knees  are  straightened.  Then 
he  shifts  his  hands  up  to  his  knees  and  proceeds  to  extend  the  hip- 
joints  by  cHmbing  up  his  thighs.  When  he  has  reached  the  upright 
position,  he  leans  his  trunk  backwards  to  keep  the  hips  extended. 


Fig.  115. — Muscular  dystrophy.     Erb's  juvenile  type. 


In  pseudo-hypertrophic  myopathy  certain  muscles  are  specially 
enlarged  and  hard — e.g.  the  calf  muscles  and  the  infra-spinati. 
Other  muscles  may  also  become  enlarged — e.g.  the  quadriceps, 
glutei,  deltoid,  biceps,  and  triceps.  On  the  other  hand,  certain 
other  muscles  waste  from  the  first,  without  any  initial  stage  of 
enlargement.     Thus  the  latissimus  dorsi,   teres  major,  and  lower 


254 


NERVOUS    DISEASES 


fibres  of  the  pectoralis  major  are  often  absent,  so  that  the  folds  of 
the  axillse  are  poorly  marked,  and  if  we  lift  up  the  child  by  the 
axillse  he  slips  through  our  grasp.     (See  Fig.  110.) 

The  enlarged  muscles  ultimately  shrink  and  become  smaller. 
As  the  calf  muscles  shorten,  they  produce  a  talipes  equinus  which 
still  further  hampers  the  walking  powers.  When  the  patient 
becomes  bedridden,  the  contractures  rapidly  attain  an  extreme 
degree.     As  the  quadriceps  wastes,  the  knee-jerk  disappears. 


Fm.  116. 


-Muscular  dystrophy.     Erb's  juvenile  type, 
endeavouring  to  rise  to  standing  posture. 


Patient 


Primary  atrophic  myopathy  is  a  less  common  type,  and  owing 
to  absence  of  muscular  enlargement,  it  is  more  likely  to  be  confused 
with  progressive  muscular  atrophy  of  spinal  origin.  At  least  three 
varieties  have  been  recognised,  according  to  the  muscles  which  are 
first  attacked.  Thus  we  have  {a)  Erb's  juvenile  type,  affecting 
the  muscles  of  the  shoulder-girdles  and  upper  arms  ;  (6)  Landouzy 
and  Dejerine's  facio-scapulo-humeral  type,  where  the  atrophy 
begins  in  the  face  ;  (c)  a  type  beginning  in  the  lower  limbs,  chiefly 
in  the  anterior  thigh  muscles. 

In  these  atrophic  varieties  there  is  no  striking  preference  for 


PARALYSIS    OF    LOWER    NEURONE    TYPE 


255 


boys  ;  both  sexes  are  equally  liable.  The  age  of  onset  too  is 
a  little  later,  commonly  between  15  and  35  years,  except  in  facial 
cases,  in  which  the  atrophy  may  come  on  in  early  childhood. 

In  Erb^s  juvenile  type  the  atrophy  begins  in  the  large  muscles 
of  the  upper  arms  and  shoulders,  especially  the  biceps,  triceps,  and 
supinator  longus.  Figs.  115,  116,  and  117  are  from  such  a  patient, 
aged  47,  who  was  a  professional  "  living  skeleton  "  in  a  travelling 


Fig.  117. — Muscular  dystrophy.     Erb's  juvenile  type, 
to  erect  posture. 


Patient  rising 


"  freak  "  show.  In  his  case  the  wasting  was  first  noticed  at  the 
age  of  19.  In  some  instances,  as  in  this  particular  case,  the  arms 
and  legs  are  attacked  about  the  same  time.  Or  the  disease  may 
begin  in  the  arms  and  spread  to  the  legs.  The  deltoids  and  spinati 
often  escape,  even  when  the  biceps  and  supinator  longus  are 
wasted,  the  condition  in  this  respect  differing  from  atrophies  of 
spinal  origin ;  and  the  forearm  muscles,  except  the  supinator 
longus,  generally  escape  too.  From  weakness  of  the  glutei  and 
quadriceps,  the  patient  when  rising  to  the  standing  posture 
may  have  to  climb   up  his  legs,  as  does  a  pseudo-hypertrophic 


case. 


256 


NERVOUS    DISEASES 


The  facio-scapulo-hum,eral  variety  of   Landouzy-Dejerine   com- 
mences in  early  life,  the  facial  muscles  being  earliest  affected.     The 


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orbiculares  oculorum^and  oris  are  weak,  so  that  the  patient  cannot 
close  his  eyes  tightly  nor  blow-out  his  cheeks  (see  Figs.  118  and 
118a).     His  lower  Hp  droops  and  projects  forwards,  and  his  mouth 


PARALYSIS    OF    LOWER    NEURONE    TYPE        257 

habitually  hangs  open.  The  smile  is  pecuharly  transverse  and  has 
a  "  forced  "  look,  the  angles  of  the  mouth  being  di'awn  outwards 
but  not  upwards.      The  tongue,  ocular  and  jaw  muscles  are  un- 


FiG.  119. — Muscular  dystrophy  ;  type  beginning  in  lower  limbs,  but 
having  advanced  to  upper  limbs.  Patient  pressing  hands  to- 
gether, to  show  atrophy  of  greater  portion  of  pectoral  muscles. 
Intrinsic  muscles  of  hands  unaffected. 

affected.     Later  the  disease  spreads  to  the  scapular  and  upper-arm 
muscles,  and  finally  to  the  spinal  muscles  and  lower  limbs. 

A  third  type  of  the  disease,  of  which  Figs.  119  and  120  show 
an  example,  begins  in  the  legs,  and  attacks  the  arms  later.  In 
this  patient  the  legs  became  weak  at  the  age  of  12.      When  she 

R 


258 


NEEVOUS    DISEASES 


came  under  observation  at  the  age  of  28  she  was  still  able  to  use 
her  arms,  which  were  contractured  at  the  elbows,  for  knitting  and 
to  feed  herself,  though  she  was  no  longer  capable  of  walking,  owing 
to  claw-foot. 

Other  Varieties  of  Muscular  Wasting. ^ — Wasting  of  muscles 
sometimes  occurs  as  a  secondary  phenomenon  in  other  diseases,  in 


Fig.  120. — Muscular  dystrophy.     Same  patient  as  in  Fig.  119. 
deformity  of  feet. 


Showing 


which  there  is  no  impHcation  of  the  spi  no -muscular  motor  neurone. 
Thus  the  muscles  may  become  small  from  disuse,  as  may  be  seen 
in  any  limb  which,  owing  to  a  fracture,  has  been  confined  for  several 
weeks  in  splints.  Disease  of  a  joint  is  generally  accompanied  by 
well-marked  atrophy  of  its  surrounding  muscles.  This  arthritic 
muscular  wasting  specially  affects  the  extensor  muscles  of  the  joint 
— for  example,  the  quadriceps  in  disease  of  the  knee-joint,  the 
interossei  in  osteo-arthritis  of  the  hands,  the  deltoid  in  disease 
of  the  shoulder-joint.     A  degree  of  muscular  wasting  also  occurs 


PARALYSIS    OF    LOWER   NEURONE    TYPE        209 

in  the  paralysed  limbs  in  ordinary  hemiplegia.  Part  of  this  may  be 
the  result  of  disuse,  but  there  are  other  cases  in  which  the  degree 
of  wasting  is  excessive,  and  disproportionate  to  the  paralysis. 
Lastly,  we  may  meet  with  marked  wasting  of  muscles  in  rare  cases 
of  hysterical  paralysis  (see  Fig.  206,  p.  404).  But  all  these 
muscular  wastings  can  be  distinguished  from  that  due  to  disease 
of  the  lower  motor  neurone  by  the  absence  of  electrical  reactions 
of  degeneration. 


CHAPTER   XV 

EECURRENT  AND   TRANSIENT   PALSIES 

There  are  certain  forms  of  motor  paralysis  which  come  and  go. 
They  tend  to  recm-  again  and  again,  and  in  the  intervals  between 
his  attacks  the  patient  is  able  to  execute  all  voluntary  movements 
in  a  normal  or  almost  normal  fashion. 

Of  these  diseases  myasthenia  gravis  is  the  most  serious.  In 
myasthenia  certain  muscles  become  infiltrated  with  deposits  of 
small  round  cells  resembhng  lymphocytes,  especially  the  striated 
muscles  innervated  by  the  upper  cranial  nerves,  though  some- 
times the  muscles  of  the  limbs  and  trunk,  and  even  the  respiratory 
muscles,  may  become  affected.  The  disease  is  characterised  by 
the  fact  that  the  patient  becomes,  even  after  very  moderate  exertion 
of  the  affected  muscles,  abnormally  easily  fatigued,  and  the  affected 
muscles  are,  for  the  time,  paralysed.  The  patient  wakes  up  in 
the  morning  practically  normal,  but  as  the  day  goes  on,  cer- 
tain muscles  gradually  become  paralysed.  Perhaps  the  muscles 
most  often  affected  are  the  levators  of  the  upper  lids.  Thus 
ptosis  appears,  often  of  unequal  degree  on  the  two  sides  (see  Fig.  121). 
To  this  may  be  superadded  an  external  ophthalmoplegia,  gener- 
ally incomplete.  The  facial  muscles  also  become  weak,  and  the 
patient  has  a  pecuUar  "  nasal "  form  of  smile,  in  which  the  angles 
of  the  mouth  are  drawn  upwards  but  very  slightly  outwards.  The 
masseters  and  other  masticatory  muscles  may  also  be  affected,  so 
that  the  patient  cannot  chew  more  than  a  few  mouthfuls.  The 
palate,  tongue  and  larynx  may  all  be  imphcated,  producing  for 
the  time  the  phenomena  of  bulbar  palsy.  In  fact,  the  disease 
was  formerly  named  "  asthenic  bulbar  paralysis."  To  correct  his 
ptosis,  the  patient  may  tilt  his  head  backwards.  But  sometimes 
the  neck  muscles  are  affected,  so  that  the  head  falls  loosely  back- 
wards or  forwards.  In  the  limbs  it  is  chiefly  the  large  proximal 
muscles  which  are  affected.  But  the  most  characteristic  feature 
is  the  transitoriness  of  the  paralysis,  and  its  recurrence  on 
shght  exertion.     Thus  the  patient  can  walk  a  short  distance,  but 

260 


RECURRENT    AND    TRANSIENT    PALSIES 


261 


soon  has  to  stop  ;  he  may  speak  a  few  sentences,  and  then  his 
voice  becomes  weak  and  his  articulation  indistinct.  In  the 
affected  muscles,  the  electrical  reactions  are  altered  and  we  have 
the  "  myasthenic  reaction."  Faradic  shocks  applied  to  the 
muscles  produce,  at  fu-st,  brisk  contractions,  but  on  repeated  stimu- 
lation the  faradic]excitability  temporarily  disappears.  In  contrast 
to  true  bulbar   palsy,  there  is  no   muscular  atrophy  as   a   rule, 


I'iG.  121. — Myasthenia  gravis  in  a  man  of  35.  Marked  weakness  of 
masseters  and  of  lower  facial  muscles  ;  also  right-sided  ptosis. 
The  patient  is  making  a  maximum  effort  to  clench  the  jaws 
and  show' the'^teeth. 


although  in  very  severe  cases,  slight  wasting  may  supervene.^ 
The  reflexes,  deep  and  superficial,  together  with  the  sphincters,  are 
unaffected.  If  the  respiratory  muscles  become  severely  affected, 
the  patient  may  die  from  respiratory  failure.  In  addition  to 
motor  phenomena  we  may  also  have  evidences  of  fatigue  in  the 
special  senses  and  even  in  common  sensibility.  Thus  the  myas- 
thenic patient  may  have  temporary  impairment  of  visual  acuity 
with  temporary  contraction  of  the  visual  fields,  and  in  rare  cases 

1  See  E.  Levi,  Rivista  di  patologia  nervosa  e  tnentale,  1906,  p.  450. 


262  NEEVOUS    DISEASES 

temporary  diminution  of   sensation   has   been   observed    in    tbe 
limbs/ 

Thomsen's  disease  or  "myotonia  congenita,"  is  a  rare  congenital 
affection  of  the  voluntary  muscles,  which  appear  to  possess  an 
excessive  proportion  of  undifferentiated  sarcoplasm  and  muscle- 
nuclei,  and  relatively  too  small  a  proportion  of  the  anisotropic  or 
fibrillar  element.  This  latter  contracts  briskly,  whereas  sarco- 
plasm contracts  very  slowly.  In  Thomsen's  disease,  whenever 
the  patient  starts  to  perform  a  brisk  voluntary  movement, 
his  muscles  are  thrown  into  a  state  of  tonic  spasm,  which 
does  not  relax  at  once  but  passes  off  gradually,  the  muscles 
slowly  becoming  supple,  until  at  length  he  can  perform  the 
movement,  say  that  of  walking,  in  a  normal  fashion  ("  ce 
n'est  que  le  premier  pas  qui  coute").  But  if  he  stops  and  starts 
again,  or  if  he  tries  to  hurry  his  original  speed,  this  stiffness 
and  slowness  of  relaxation  reappear,  and  have  again  to  be,  as  it 
were,  worked  off.  The  lower  limbs  are  most  commonly  affected, 
the  affected  muscles  often  being  somewhat  enlarged,  but  other 
muscles  may  also  show  the  phenomena.  Thus  the  patient's  eyes 
may  remain  for  a  time  firmly  closed  after  a  cough  or  sneeze,  his 
mouth  may  remain  open  after  a  yawn,  and  so  on.  The  sensory 
functions  are  unaffected.  The  reflexes  are  normal  in  type,  but 
sometimes  when  the  plantar  reflex  is  elicited  the  muscles  of  the 
toes  remain  tonically  flexed  for  several  seconds,  instead  of  relaxing 
promptly  as  in  health.  A  similar  myotonic  condition  may  also 
be  observed  in  the  cremasteric  reflex.  The  affected  muscles  have  a 
characteristic  reaction  to  electrical  stimulation.  Their  excitabihty 
is  increased  to  both  faradism  and  galvanism.  To  galvanism 
KCC  is  equal  to  ACC  (instead  of  being  greater,  as  in  health), 
and  the  contraction  set  up,  whether  by  galvanism  or  by  fara- 
dism, is  remarkably  persistent,  lasting  for  a  time  after  the  stimulus 
has  ceased.  The  disease  runs  in  families  and  affects  patients  of 
both  sexes. 

Eulenberg's  disease  or  "paramyotonia  congenita,"  is  a  family 
affection  somewhat  like  Thomsen's  disease,  in  which  a  tonic  spasm 
appears  in  certain  voluntary  muscles,  more  particularly  in  the  face, 
so  that  the  patient  is  unable,  for  a  quarter  of  an  hour  or  longer, 
to  open  his  eyes  or  to  speak.  Less  often  the  muscles  of  the 
limbs  are  affected.     However,  the  condition  differs  from  Thomsen's 

^  Tilney  and  Mitchell  Smith,  Ncurorjraplis,  1911,  vol.  i.  p.  178. 


RECURRENT    AND    TRANSIENT    PALSIES  263 

disease  in  its  immediate  exciting  cause.  The  tonic  spasm  of 
Eulenberg's  disease  is  excited  not  by  exertion  but  by  cold,  and 
is  generally  relieved  by  warmth.  The  two  diseases,  however,  are 
closely  aUied,  and  have  been  observed  coincidently  in  members  of 
the  same  family.^ 

Myotonia  atrophica'-  is  a  rare  disease,  intermediate  in  its 
characters  between  the  myotonias  and  the  myopathies.  It  some- 
times occurs  in  several  members  of  the  same  family.  The  patients 
are  more  often  males  than  females,  and  the  symptoms  usually 
appear  in  adult  life.  A  considerable  proportion  of  patients  also 
show  family  cataract.  The  myotonic  phenomena  generally  pre- 
cede the  muscular  wasting.  The  first  symptom  is  usually  a  difficulty 
in  relaxing  the  grasp,  e.g.  after  shaking  hands.  Myotonic  phenomena 
in  other  muscles  are  slighter  in  degree,  and  are  chiefly  seen  in  the 
muscles  of  mastication,  the  facial  muscles  and  the  tongue ;  they 
are  rare  in  the  lower  limbs.  Atrophy  of  myopathic  type  appears 
later,  irregular  in  its  distribution,  chiefly  affecting  the  facial 
muscles  (resembling  the  Landouzy-Dejerine  type  of  myopathy),  the 
sterno -mastoids  and  the  vasti  muscles  of  the  thighs.  It  may  also 
be  present  elsewhere  in  lesser  degree,  as  in  the  forearm  muscles  and 
the  dorsiflexors  of  the  foot.  The  electrical  reactions  in  the  wasted 
muscles  are  simply  diminished. 

Another  interesting  variety  of  transient  paralysis  is  known  as 
intermittent  arterial  claudication  or  "dysbasia  angio-sclerotica " 
("  claudication  inter mittejite "  of  Charcot,  or  the  "  intermit- 
tirendes  Hinken "  of  German  authors).  The  patient  is  most 
commonly  a  man  of  middle  age,  sometimes  of  gouty  con- 
stitution, who  very  often  has  been  an  inveterate  tobacco-smoker. 
The  symptoms  are  very  characteristic.  At  rest  he  feels  no 
disability.  But  when  he  begins  to  walk,  although  he  starts 
off  normally,  he  soon  begins  to  feel  his  legs  tired,  heavy  and 
painful.  A  cramp-like  pain  appears  and  gradually  becomes 
intolerable,  maldng  him  limp ;  and  if  he  perseveres  with  his 
attempt,  he  finally  becomes,  for  the  time,  totally  unable  to 
walk  a  single  step.  He  rests,  the  pain  and  weakness  pass  off, 
only  to  return  when  he  starts  to  walk  afresh.  If  we  examine  such 
a  patient  during  a  paroxysm  of  temporary  incapacity,  we  find 

1  Delprat,  Deutsche  med.  Wochenschnft,  1892,  s.  158. 

^  Rossolimo,  Nouvdle  Iconofiraphie  de  la  Salpctrierc,  1902,  p.  63.  Batten  and 
Gibb,  Brain,  1909,  p.  187.  Bramwell  and  Addis,  Edin.  Med.  Journal,  July 
1913,  p.  21. 


264  NERVOUS    DISEASES 

his  feet  and  legs  cold,  and  perhaps  purple  or  mottled  red.  But 
what  is  most  characteristic  of  all  is  that  the  pulse  in  the  feet,  in 
the  posterior  tibial  or  the  dorsalis  pedis  artery,  is  absent  or  nearly  so. 
There  are  no  sensory  changes,  the  reflexes  are  normal,  and,  except 
during  the  paroxysms,  the  motor  power  of  the  limbs  is  unimpaired. 
Goldflani's  sign  can  often  be  ehcited,  consisting  in  marked  pallor 
of  the  foot,  and  sometimes  of  the  lower  part  of  the  leg,  when  the 
patient,  lying  horizontal,  with  the  leg  extended,  repeatedly  raises 
it  at  the  hip-joint.  All  these  phenomena  appear  to  be  the  results 
of  a  temporary  spasm  of  the  arteries  of  the  limb  (the  arteries 
themselves  often  being  already  narrowed  by  arterio-sclerosis),  so 
that  during  walking  an  increased  blood-supply  to  the  muscles  is 
not  forthcoming,  hence  there  result  temporary  ansemia,  pain  and 
weakness  in  the  affected  muscles.  In  rare  instances  similar  pheno- 
mena have  been  observed  in  the  arms. 

Intermittent  spinal  claudication,  due  to  spasm  of  the  arteries 
of  the  spinal  cord,  also  occurs.  As  in  peripheral  claudication,  the 
symptoms  occur  on  exertion.  As  a  rule  one  leg  is  affected  sooner 
than  the  other,  and  the  malady  may  even  remain  unilateral  for 
months  or  years.  After  walking  a  certain  distance,  say  a  mile  or 
two,  the  patient  develops  temporary  asymmetrical  weakness  of 
the  lower  limbs,  of  spastic  type,  with  exaggerated  deep  reflexes, 
extensor  plantar  responses  and  delay  or  precipitancy  of  micturi- 
tion. As  the  malady  progresses,  the  amount  of  exertion  necessary 
to  induce  the  symptoms  becomes  less  and  less,  until  the  patient 
becomes  unable  to  walk  more  than  a  few  steps  without  developing 
spastic  paraplegia.  Moreover  the  spinal  arteries  ultimately  undergo 
organic  obstruction  by  arteritis  (often  of  syphilitic  origin),  pro- 
ducing not  merely  intermittent  but  permanent  spastic  paraplegia. 
The  condition  is  distinguished  from  intermittent  arterial  claudica- 
tion by  the  absence  of  coldness  or  blueness  of  the  feet,  by  the 
occurrence  of  a  sensation  of  heaviness  rather  than  pain  in  the 
limbs,  by  the  alteration  of  the  reflexes  and  by  the  bladder  affection. 

Cases  also  occur  in  which  a  hemiplegia,  partial  or  complete, 
sometimes  accompanied  by  aphasia,  occurs  in  an  elderly  patient, 
indistinguishable  at  first  from  an  ordinary  cerebral  haemorrhage 
or  thrombosis.  But  within  a  few  hours  all  the  hemiplegic  pheno- 
mena disappear  suddenly,  leaving  the  patient  apparently  normal. 
The  patient  may  have  a  series  of  such  attacks  of  transient  hemi- 
plegia at  intervals  of  days,  weeks  or  months.     For  over  three  years 


RECURRENT    AND    TRANSIENT    PALSIES         265 

I  watched  the  case  of  an  elderly  cabman  who  had  numerous 
attacks  of  left  hemiplegia  lasting  for  a  day  or  so,  leaving  him 
absolutely  well  in  the  intervals.  Another  case  of  mine  was  in  a 
vigorous  business  man,  aged  fifty-one,  who  had  frequent  attacks 
of  temporary  aphasia  with  right  hemiplegia.  Similar  cases  have 
also  been  recorded  by  Grasset  ^  and  by  Langwill."^  Such  cases 
may  be  termed  angio-spastic  hemiplegia  or  intermittent  cerebral 
claudication,  and  are  probably  due  to  temporary  spasm  of  one 
middle  cerebral  artery,  analogous  to  the  spasm  of  peripheral 
vessels  in  intermittent  limp.  They  must  be  carefully  distinguished 
from  the  transient  hemiplegia  which  is  not  uncommon  in  general 
paralysis  of  the  insane.  Sometimes  these  transient  attacks  culmi- 
nate in  a  final  attack  of  hemiplegia  which  does  not  clear  up  but 
remains  permanent,  due  to  actual  arterial  thrombosis.'^  In  the 
business  man  above  referred  to,  this  occurred  two  and  a  half  years 
after  the  first  attack  of  his  series. 

Amongst  the  transient  paralyses  we  must  also  bear  in  mind  the 
various  craft-palsies,  professional  cramps,  or  occupation  neuroses,  in 
which  the  limb  is  normal  for  all  motor  actions  except  one  particular 
movement — often,  unfortunately,  the  one  on  which  the  patient's 
livelihood  depends.  The  commonest  variety  is  the  so-caUed  writer's 
cramp  or  scrivener's  palsy,  though  we  also  meet  with  similar  con- 
ditions in  the  cramp  of  pianists,  vioUnists,  telegraphists,  typists, 
tailor's  cutters,  hair-cutters,  hammer-men,  cow-milkers,  watch- 
makers, harpists,  cigarette-makers,  sempstresses,  and  so  on.  The 
cramp  comes  on,  not  during  the  period  when  the  sufferer  is  learning 
his  occupation,  but  after  he  has  become  an  expert  and  requires  to 
perform  the  particular  skilled  movement  repeatedly  over  prolonged 
periods.  For  all  other  movements  except  that  particular  one,  the 
limb  is  normal.  Thus  in  writer's  cramp  the  patient  can  use 
his  hand  normally  for  piano -playing  or  for  grasping  and  using  a 
heavy  tool.  This  is  because  the  weakness  is  not  due  to  muscular 
but  to  cerebral  fatigue.  A  professional  cramp  does  not  appear  in 
its  fully  developed  form  at  first,  but  passes  through  different  stages 
of  severity.  In  the  shghtest  variety  there  is  simply  a  degree  of 
stiffness  or  spasm  in  performing  the  act,  with  a  subjective  sensation 
of  pain  and  of  intense  mental  discomfort  and  fatigue.    In  other  cases 

^  Revue  neurologique,  May  30,  1906. 
2  Scottish  Medical  and  Surgical  Journal,  June  1906. 

^  See  a  case  by  Hunter  and  Robertson,  Review  of  Neurol,  and  Psych.,  1913, 
p.  419. 


266  NERVOUS    DISEASES 

a  temporary  paralysis  appears  when  the  patient  attempts  to  write, 
so  that  the  pen  can  no  longer  be  held  in  the  hand.  In  still  more 
severe  cases  tremor  is  superadded  to  spasm  in  the  affected  muscles. 
The  diagnosis  is  easy,  inasmuch  as  the  phenomena,  whether  spastic 
or  paralytic  or  perhaps  a  combination  of  both,  only  supervene  when 
the  one  skilled  motor  action  is  performed,  and  the  same  muscles 
can  be  used  for  all  other  actions  without  pain,  spasm  or  weakness. 

There  is  also  a  curious  hereditary  disease  known  as  "family 
periodic  paralysis."  This  malady  may  run  through  several  suc- 
cessive generations  of  the  same  family,  attacking  one  or  more 
members  of  the  same  generation.  Males  and  females  are  both 
liable.  The  patient,  who  is  otherwise  apparently  healthy,  has 
attacks  of  flaccid  paralysis  of  all  four  limibs,  recurring  irregularly 
without  apparent  exciting  cause.  The  duration  of  a  paroxysm 
varies  from  two  or  three  days  down  to  a  few  hours.  The  attacks 
generally  come  on  during  the  night  when  the  patient  is  in  bed. 
He  wakes  up  and  finds  himself  more  or  less  widely  paralysed. 
First  the  legs  are  affected,  later  the  arms,  and  last  of  all  the 
muscles  of  the  trunk  and  neck.  The  cranial  nerves  usually  escape. 
In  the  Hmbs  the  paralysis  starts  proximally  and  the  distal  parts 
are  affected  last,  so  that  the  patient  may  still  be  able  to  move 
his  toes  and  fingers  when  he  has  lost  all  power  in  the  hips  and 
shoulders.  In  severe  cases  the  intercostal  muscles  may  also  be 
paralysed.  Most  striking  of  all  is  the  fact  that  during  these 
paroxysms  of  flaccid  palsy  the  affected  muscles  lose,  for  the  time, 
their  excitability  to  faradic,  galvanic,  or  mechanical  stimulation 
(cadaveric  reaction),  and  all  the  reflexes  in  the  affected  hmbs  dis- 
appear. Sensation  is  unimpaired  and  the  sphincters  are  unaffected. 
An  additional  point  is  that  during  the  paroxysm,  the  left  ventricle 
becomes  temporarily  dilated,  as  can  be  proved  by  percussion  and 
occasionally  by  the  appearance  of  a  systolic  mitral  bruit.  The 
muscular  paralysis  passes  off  in  the  reverse  order  to  that  in 
which  it  came  on.  The  toes  and  fingers  recover  before  the  proxi- 
mal muscles,  and  the  muscles  earliest  attacked  are  the  last  to 
recover.  The  patient  then  remains  apparently  normal  until  his 
next  attack,  weeks  or  months  later. 

Sudden  attacks  of  hemiplegia  may  also  occur  in  general 
paralysis  of  the  insane,  constituting  a  variety  of  so-called  "  con- 
gestive attacks."  But  although  the  patient  may  recover  rapidly 
from  his  hemiplegia,  often  within  a  few  days,  he  is  not  a  normal 


KECURRENT    AND    TRANSIENT    PALSIES         267 

individual,  for  careful  physical  examination  will  always  reveal 
evidences  of  the  disease,  mental  or  physical,  e.g.  facial  tremors, 
pupillary  changes,  or,  most  constant  of  all,  lymphocytosis  of  the 
cerebro-spinal  fluid. 

Amongst  other  transient  affections  we  may  mention  those 
of  muscular  cramp  and  of  tetany.  The  conditions  are  easily 
recognised,  and  may  temporarily  interfere  with  the  movements 
of  the  affected  limbs.  Both  are  painful  affections,  tetany  being 
most  commonly  seen  in  infants,  whilst  cramp  is  most  often  met 
with  in  healthy  adolescents  or  adults  who  have  been  performing 
some  unwonted  prolonged  muscular  effort.  Cramp  is  also  a 
distressing  symptom  in  cholera,  in  some  cases  of  diabetes,  and 
occasionally  in  exophthalmic  goitre.  Tetany  is  generally  bilateral, 
and  produces  a  characteristic  posture  of  the  hands  and  feet  (see 
Eig.  39,  p.  85). 

Occasionally  we  see  patients  who  complain  that  their  legs 
suddenly  give  way  in  the  street,  causing  them  to  fall.  This  may 
be  due  to  various  causes.  For  example,  it  is  a  not  uncommon 
symptom  in  tabes.  The  tabetic  patient  often  has  hypotonia  of 
the  muscles  about  the  knees  and  also  deficient  joint-sense,  a  com- 
bination of  phenomena  which  may  make  him  fall  unexpectedly. 
In  such  a  case  the  condition  of  the  deep  reflexes,  the  state  of  the 
pupils,  and  the  other  phenomena  of  tabes  render  the  diagnosis 
easy.  Other  cases  of  sudden  falling  are  due  to  minor  epilepsy, 
where  the  patient  has  an  attack  of  momentary  unconsciousness 
during  which  he  falls,  but  recovers  consciousness  at  once  and  gets 
up  again,  not  knowing  why  he  has  fallen.  Here  the  diagnosis 
will  depend  on  the  observation  of  other  epileptiform  attacks,  major 
or  minor.  We  should  particularly  inquire  for  the  occurrence  of 
sudden  pallor  of  the  face  or  fixity  of  expression,  indicating  a  passing 
attack  of  petit  mal,  too  slight,  perhaps,  to  produce  a  fall. 

In  other  cases,  again,  we  have  to  do  with  sudden  vertigo, 
as  in  Meniere's  disease,  causing  the  patient  to  fall.  Such  cases 
are  recognised  by  the  concomitant  auditory  phenomena  (see  p.  170), 
and  by  the  fact  that  they  are  not  associated  with  loss  of 
consciousness. 

Sudden  weakness  of  a  limb  may  occur  in  hysteria,  especially 
after  some  emotional  shock.  Hysterical  paralysis  may  persist 
for  variable  periods  of  time,  varying  from  a  few  hours  to 
many    weeks     or     months.       The    paralysis    not    uncommonly 


268  NERVOUS    DISEASES 

passes  off  as  suddenly  as  it  came  on,  sometimes  under  emotional 
or  religious  excitement,  under  hypnotic  suggestion,  or  under 
energetic  stimulation,  electric  or  thermal,  for  example,  that  of 
a  PacqueUn  cautery.  Hysterical  paralysis  never  attacks  a  single 
muscle,  but  always  a  group  of  muscles.  It  is  never  accom- 
panied by  reactions  of  degeneration,  no  matter  how  much  the 
hysterical  limb  may  be  wasted.  We  diagnose  hysteria  by  a 
process  of  exclusion,  noting  not  only  the  absence  of  certain  signs 
of  organic  disease,  but  looking  also  for  the  presence  of  various 
hysterical  "  stigmata,"  to  which  we  shall  refer  later. 

But  we  must  not  forget  that  in  many  cases  of  apparently 
hysterical  and  transient  paralysis  in  young  women,  the  patient 
after  one  or  more  of  such  attacks  may  afterwards  develop  the 
signs  of  disseminated  sclerosis.  The  onset  of  disseminated  sclerosis 
may  be  indistinguishable  from  an  attack  of  hysterical  paralysis, 
the  weakness  of  the  limb  in  both  diseases  may  be  transient  and 
may  apparently  clear  up  completely  for  a  time.  But  a  series  of 
such  attacks  should  always  raise  in  our  minds  the  suspicion  of  an 
underlying  disseminated  sclerosis  and  should  make  us  give  a  guarded 
prognosis,  especially  if  the  patient  has  had  more  than  one  attack 
of  weakness,  not  necessarily  in  the  same  limb.  We  should  pay 
particular  attention  to  the  state  of  the  optic  discs.  Early  optic 
atrophy  will  exclude  mere  hysteria,  so  also  will  an  extensor 
plantar  reflex  or  anything  approaching  a  true  nystagmus.  In 
fact,  the  disease  which  is  most  often  wrongly  diagnosed  as  hysteria 
is  incipient  disseminated  sclerosis. 


CHAPTEK    XVI 

INCO-ORDINATION 

A  NEWLY-BORN  cMld  cannot  co-ordinate  the  movements  of  its 
limbs.  Certain  co-ordinated  vital  actions,  such  as  sucking,  swallow- 
ing, respiration,  &c.,  are  performed  well  from  birth,  but  in  an 
infant's  limbs  the  movements  are  mostly  of  an  aimless  restless 
character,  with  the  exception,  perhaps,  of  grasping  movements  of 
the  hands.  And  even  these  latter  differ  from  the  co-ordinated 
grasp  of  later  Hfe,  inasmuch  as  the  infant's  thumb  is  hardly  used 
at  all  for  opposition,  and  the  flexion  movement  of  the  fingers 
occurs  chiefly  when  some  object  comes  in  contact  with  the  hand, 
the  movement  being  reflex  rather  than  voluntary. 

The  child  only  learns  after  long  practice  to  use  its  muscles  in 
such  a  fashion  as  to  produce  properly  co-ordinated  movements  of 
the  limbs.  Walking,  writing,  swimming,  the  playing  of  any  game, 
are  all  performed  awkwardly  at  first.  Skill  is  at  last  attained 
by  frequent  repetition,  and  once  a  co-ordinated  action  has  been 
thoroughly  learned,  the  effort  for  its  performance  becomes  in- 
finitesimal, so  that  in  time  it  is  performed  more  or  less  auto- 
maticaUy. 

Every  co-ordinated  action  involves  contraction  not  only  of  the 
so-called  prime-movers  but  of  their  antagonists,  and  if  these  two 
groups  are  not  properly  balanced,  the  attempted  movement  is 
awkward  and  jerky.  This  condition  occurs  in  a  number  of  diseases 
and  is  termed  ataxia  or  incoordination.  This  means  clumsiness, 
unsteadiness,  or  awkwardness  in  the  performance  of  movements  in 
a  non-paralysed  patient  who  was  previously  able  to  execute  these 
movements  in  normal  fashion. 

In  testing  for  ataxia  of  the  upper  limbs,  we  ask  the  patient 
to  perform  such  an  action  as  picking  up  a  small  object,  say 
a  pin,  from  a  smooth  surface.  If  he  is  ataxic,  he  fumbles 
during  the  attempt,  or  may  perhaps  pounce  on  the  object  in  a 
sudden,  jerky  fashion.  Another  useful  test  is  to  ask  the  patient 
to  lift  a  brimming  glass  of  water  to  his  lips  and  notice  whether 

269 


270  NERVOUS    DISEASES 

he  spills  it.  Or  we  may  ask  him  to  touch,  rapidly  the  tip  of  his 
nose  with  each  index  finger  in  succession.  If  he  is  ataxic,  his 
finger  misses  his  nose  by  a  greater  or  smaller  interval,  or,  on 
reaching  it,  the  finger  shows  additional  oscillatory  movements. 
Other  good  tests  for  ataxia  are  to  make  the  patient  button  or 
unbutton  his  coat  or  collar,  or  to  write  with  a  fine-pointed  pen. 
In  every  case,  we  should  observe  whether  the  unsteadiness  is 
increased  or  unchanged  when  the  patient  shuts  his  eyes.  Shght 
degrees  of  ataxia  due  to  sensory  impairment  may  be  noticeable 
only  when  the  patient  is  deprived  of  the  help  of  his  visual 
impressions. 

In  the  case  of  the  lower  limbs  we  detect  moderately  severe 
ataxia  by  observing  the  patient's  gait,  asking  him  to  walk 
"  heel-and-toe  "  along  a  straight  line,  then  to  turn  sharply  and 
come  back.  In  well-marked  locomotor  ataxia  the  gait  is  broad- 
based,  the  feet  are  lifted  too  high  and  the  heels  are  brought  down 
with  a  stamp.  In  cerebellar  disease,  on  the  other  hand,  the 
patient  reels  or  lurches  along,  being  especially  unsteady  when 
turning  round  (see  later,  "Postures  and  Gaits").  To  detect 
ataxia  of  a  single  lower  limb,  we  ask  the  patient  to  place  one  heel 
on  the  opposite  knee,  or  to  trace  with  one  foot  a  circle  or  some 
other  pattern  on  the  floor,  or  we  ask  him  when  lying  down  to 
touch  with  his  toe  our  own  finger  held  in  the  air.  And  here  also, 
in  ataxia  of  the  lower  hmbs,  we  should  always  note  whether  the 
patient's  unsteadiness  is  increased  or  unchanged  by  shutting  the 
eyes.  In  tabetic  ataxia  of  the  lower  Hmbs,  the  unsteadiness  is 
increased  when  the  eyes  are  shut.  Romberg^ s  sign  consists  in  the 
tendency  of  a  patient,  who  can  stand  steadily  with  the  eyes  open, 
to  fall  when  he  closes  them.  Thus  an  early  sign  of  tabes  is  the 
so-called  "  wash-basin "  sign,  where  the  patient  falls  into  his 
basin  when  washing  his  face.  A  minor  degree  of  Romberg's  sign 
can  often  be  detected  in  the  earlier  stages  of  tabes,  where  the 
patient  is  still  able  to  stand  with  the  eyes  shut,  but  the  tendons 
on  the  dorsum  of  the  foot  are  seen  to  exhibit  irregular  restless 
contractions,  the  so-called  "  danse  des  tendons." 

Ataxia  of  the  bulbar  muscles  has  already  been  referred  to  (see 
Dysarthria,  p.  122).  As  to  ataxia  of  the  muscles  of  the  trunk, 
its  diagnostic  significance  is  less  than  that  of  the  limbs,  inasmuch 
as  by  the  time  that  the  trunk  muscles  are  recognisably  ataxic,  the 
limbs   already   show   very  marked   unsteadiness.     Ataxia   of  the 


INCO-ORDINATION  271 

head  and  trunk  muscles  is  evidenced  by  swaying  movements  when 
the  patient  sits  up. 

Having  detected  ataxia  in  the  movements  of  any  limb,  we  must 
always  determine  the  condition  of  the  sensory  impulses  from  that 
limb,  testing  not  only  the  various  forms  of  cutaneous  sensibility 
but  also  the  deep  sensations,  especially  the  kinaesthetic  sense  and, 
still  more  important,  the  joint-sense.  Finally,  we  must  determine 
the  condition  of  the  deep  reflexes,  noting  their  exaggeration  as  in 
disseminated  sclerosis,  or  their  abohtion  as  in  tabes  or  in  Friedreich's 
ataxia.     We  also  note  the  type  of  plantar  reflexes. 

The  commonest  variety  of  ataxia  is  that  due  to  deficiency  of 
peripheral  impressions — not  so  much  from  the  skin  as  from  the 
deeper  structures,  the  muscles  and  joints.  Thus  in  lesions  of  feri- 
flieral  sensory  nerves  an  anesthetic  limb  is  often  ataxic.  Division 
of  the  posterior  roots  of  the  brachial  plexus,  the  anterior  roots  re- 
maining intact,  causes  marked  ataxia  of  the  upper  limb.  In  fact 
such  a  patient  may  be  totally  unable  to  move  the  limb  if  his  eyes 
are  closed,  so  that  he  no  longer  has  the  guiding  influence  of  vision. 
Degeneration  of  the  posterior  roots  and  posterior  columns,  as 
in  tahes,  produces  marked  ataxia.  A  tabetic  patient  is  ataxic 
because  of  deficiency  of  afferent  impressions,  more  especially  from 
his  muscles  and  from  his  joints.  If  the  muscle-tonus  is  lost  and 
the  muscles  are  hypotonic,  as  in  many  cases  of  tabes,  the  patient 
has,  as  it  were,  to  "  pull  in  the  slack  "  before  the  muscles  come 
into  proper  play,  thereby  making  the  movement  jerky,  inharmonious, 
and  flail-like.  Joint-sense  being  impaired,  he  has  to  perform 
an  exaggerated  movement  in  order  to  get  the  sensation  of  having 
moved  the  joint  at  all.  Thus  in  walking  when  he  lifts  his  leg, 
owing  to  want  of  proper  joint-sense,  he  throws  the  limb  up  with 
abnormal  suddenness  and  to  an  unnecessary  height  in  order  to 
gain  the  sensation  of  flexion  of  the  joint.  He  then  stamps 
it  down  with  excessive  emphasis  to  make  sure  that  it  really 
is  extended.  Such  a  patient  with  ataxia  of  sensory  origin  com- 
pensates for  the  deficiency  of  sensory  impressions  from  his  limbs 
by  means  of  his  vision.  When  watching  his  partially  ansesthetic 
limbs,  he  can  control  them  better.  Hence  if  he  closes  his  eyes, 
the  regulating  influence  of  vision  is  lost  and  he  becomes  much 
more  ataxic.  This  is  the  probable  explanation  of  Eomberg's 
sign  in  tabes. 

Ataxia  similar  to  that  of  tabes  also  occurs  in  other  organic 


272  NERVOUS    DISEASES 

cord  lesions  implicating  the  posterior  columns,  as,  for  instance,  in 
tumours  or  chronic  sclerosis  of  the  posterior  columns,  whether  com- 
bined or  not  with  lateral  sclerosis — e.g.  some  cases  of  disseminated 
sclerosis  or  spinal  syphilis.  In  such  diseases  the  other  signs  and 
symptoms  guide  us  to  a  correct  diagnosis. 

Ataxia  combined  with  spasticity  occurs  in  the  early  stage  of 
subacute  combined  degeneration  of  the  spinal  cord,  generally  a 
disease  of  middle  life.  This  disease  occurs  chiefly  in  conditions  of 
profound  anaemia.  In  the  &st  stage  of  the  malady  joint-sense  is 
lost  and  there  are  subjective  sensations  of  tingling  in  the  lower 
limbs,  not  unlike  those  of  tabes,  but  with  increased  knee-jerks  and 
extensor  plantar  reflexes.  Vibration-sense  in  the  bones  of  the 
lower  limbs  is  lost  long  before  any  cutaneous  anaesthesia 
develops.  After  lasting  for  weeks  or  months  the  disease 
then  changes  its  type,  and  in  this  second  stage  the  spastic 
paraplegia  becomes  severe  and  marked  anaesthesia  develops  in 
the  lower  limbs  and  trunk.  Lastly,  and  usually  abruptly,  within 
a  few  days  the  type  changes  once  more,  and  there  is  a  terminal 
stage  of  flaccid  paraplegia  lasting  a  few  weeks,  with  absolute 
anaesthesia  of  the  lower  limbs  and  trunk,  loss  of  the  knee-jerks, 
the  plantar  reflexes  remaining  extensor  in  type.  The  paralysed 
muscles  rapidly  waste  and  lose  their  faradic  excitability.  The 
bladder  and  rectum  are  uncontrolled  and  the  lower  limbs  become 
oedematous.  The  whole  disease  from  start  to  finish  lasts  about 
two  or  three  years. 

Vestibular  Ataxia. — A  highly  characteristic  disorder  of  co- 
ordination appears  temporarily  in  healthy  individuals  during  the 
transient  vestibular  nystagmus  produced,  according  to  Biirany's 
method,  by  syringing  the  external  auditory  meatus  with  cold  or 
hot  water,  by  rotating  the  patient  in  a  revolving  chair,  or  by  the 
stimulation  of  a  galvanic  current  transmitted  between  the  two 
mastoid  processes.  The  effect  produced  is  known  as  Bdrany's 
"  vorhei-zeigen,'^  signifying  deviation  or  misdirection  in  pointing 
to  an  object.  It  is  ehcited  as  follows  : — The  patient,  with  closed 
eyes,  touches  the  physician's  finger  held  steadily  in  front  of  him. 
He  is  now  directed,  without  opening  his  eyes,  to  drop  his  arm 
vertically  and  to  come  up  again,  so  as  once  more  to  touch  the 
physician's  finger,  which  forms  the  target.  A  normal  person 
should  succeed  in  touching  the  target  with  his  eyes  closed,  on 
testing  with  either  hand.     The  experiment  is  then  repeated,  but 


INCO-ORDINATION  273 

this  time  the  patient  approaches  the  target  along  a  horizontal 
plane,  from  side  to  side.  Here  also  the  normal  person  succeeds 
without  difficulty  with  either  hand.  After  these  preliminaries, 
by  syringing  the  left  ear  with  cold  water  (the  patient  meantime 
lying  on  his  back),  we  now  proceed  to  induce  a  horizontal  nystagmus 
in  the  patient  when  he  looks  towards  the  right.  When  we  try 
the  pointing  tests  again,  we  now  find  deviation  or  mispointing 
(vorbei-zeigen)  of  all  the  patient's  limbs  towards  the  left,  so  that 
the  patient's  finger  passes  to  the  left  of  the  target  by  several  inches, 
i.e.  he  misses  towards  the  direction  of  the  slow  phase  of  the 
nystagmus.  If  we  produce  a  vestibular  nystagmus  on  looking 
downwards  (the  slow  phase  being  upwards),  we  have  deviation  of 
all  the  limbs  in  an  upward  direction.  If  we  produce  a  rotatory 
nystagmus  on  looking  to  the  right,  the  left  arm  shows  deviation 
downwards,  whilst  the  right  arm  deviates  upwards,  on  testing  in 
the  horizontal  side-to-side  plane. 

This  mispointing  or  "  vorbei-zeigen "  depends  not  only  on  the 
nystagmus  but  also  on  the  position  of  the  head.  By  changing  the 
posture  of  the  head  we  can  correspondingly  alter  the  line  of  deviation. 
Thus,  during  a  horizontal  nystagmus  towards  the  right,  if  the  head 
be  suddenly  bent  through  a  right  angle,  on  to  the  right  shoulder,  the 
deviation  to  the  left  disappears  and  is  replaced  by  deviation  upwards. 
Again,  during  a  rotatory  nystagmus  towards  the  right,  if  we  rotate 
the  head  around  a  vertical  axis  through  a  right  angle  towards  the  right, 
the  deviation  in  the  frontal  plane  disappears,  and  is  replaced  by  devia- 
tion in  the  mesial  plane,  so  that  both  arms  deviate  downwards.^ 

A  patient  may  be  ataxic  when  all  his  peripheral  sensations 
are  normal.  This  occurs  in  the  different  varieties  of  cerebellar 
ataxia.  Let  us  take,  for  example,  Friedreich's  ataxia,  a  develop- 
mental disease  affecting  mainly  the  afferent  tracts  in  the  cord 
leading  upwards  to  the  cerebellum,  which  is  the  centre  for  auto- 
matic co-ordination  (the  cerebellum  itself  being  intact).  In 
Friedreich's  ataxia  the  patient  becomes  ataxic,  as  in  tabes,  but 
in  the  early  stages  of  the  disease  there  may  be  no  sensory  loss  of 
any  kind.  The  ataxia  is  unaffected  by  closing  the  eyes.  As  the 
disease  advances  and  the  degeneration  of  the  posterior  columns 
becomes  more  profound,  those  sensory  impressions  which  run 
upwards  in  the  posterior  columns  {i.e.  joint-sense,  kinsesthetic 
sense,   and  vibration  sense)  become  lost,   and  slight  tactile  loss 

1  Barany,  Wiener.  Bin.  Wochensch.,  1912,  pp.  2033-38. 

S 


274 


NERVOUS    DISEASES 


occurs  in  the  distal  portions  of  the  limbs,  the  lower  limbs  being 
earlier  and  more  severely  affected  than  the  upper,  whilst  sensi- 
bility to  temperature  and  pain,  running  upwards  in  the  lateral 

columns,  remains  unimpaired  to 
the  end.i  The  age  of  the  patient, 
who  is  commonly  an  adoles- 
cent, the  presence  of  scoHosis,  of 
manus  cava,  and  of  pes  cavus 
(Figs.  122  and  123),  the  normal 
pupillary  reactions,  the  presence 
of  nystagmus,  the  absence  of 
lightning  pains  or  of  bladder 
trouble,  all  serve  to  distinguish 
this  disease  from  tabes,  though 
in  both  diseases  the  deep  re- 
flexes are  absent.  The  plantar 
reflexes  in  tabes  are  flexor  in 
type,  whilst  in  Friedreich's  ataxia 
they  are  of  the  extensor  variety, 
and  associated  with  well-marked 
"defensive  reflexes." 

Well-marked  ataxia  combined 
with  muscular  atrophy,  absence 
of  deep  reflexes,  and  deformity 
of  the  feet  and  hands,  also  occur 
in  family  progressive  hypertrophic 
neuritis  (see  above,  p.  238).  In 
this  disease,  however,  unlike 
Friedreich's  ataxia,  we  never 
have  an  extensor  plantar  reflex, 
whilst  from  the  start  there  are 
well-marked  sensory  changes  in 
the  limbs. 

Ataxia  also  occurs  in  certain 
locaUsed  lesions  of  the  medulla 
oblongata.  Thus,  for  example,  a  unilateral  lesion  may  interrupt 
the  fibres  of  the  direct  cerebellar  tract  and  thereby  interfere  with 
co-ordination  of  the  ipso-lateral  limbs.  Such  a  lesion  (com- 
monly   the   result    of    thrombosis   of  the   posterior   inferior  cere- 

^  Saunders,  Brain,  vol.  xxxvi.  1913,  p.  166. 


Fig.  122. 


-Friedreich's  ataxia, 
scoliosis. 


Showing- 


INCO-ORDINATION 


275 


bellar  artery),  which  usually  interrupts  at  the  same  time  the  fibres 
of  Growers'  tract,  may  extend  inwards  to  implicate  the  inter-olivary 
arcuate  fibres  and  the  fiJlet,  together  with  the  nuclei  of  the  lower 
cranial  nerves.  It  produces  a  characteristic  unilateral  bulbar 
syndrome.'     The  symptoms  are  as  follows  : — From  interruption  of 


Fig.  123. — Friedreich's  ataxia.     Showing  pes  cavus  and  manus  cava. 

the  cerebellar  afferent  fibres  there  is  ataxia  (or  asynergia)  of  the 
ipso-lateral  limbs.  From  interference  with  the  tract  for  pain  and 
temperature  we  have  analgesia  and  therm-ansesthesia  of  the 
opposite  side  of  the  body  (see  Fig.  12,  p.  18).  From  inter- 
ference with  the  oculo-pupillary  centre  in  the  bulb  there  is 
myosis  and  pseudo-ptosis  (see  later,  "  Cervical  Sympathetic 
Paralysis,"  p.  359),  and  there  may  be  difficulty  of  deglutition  due 

1  Babinski  and  Nageotte,  Revue  neurologique,  1902,  p.  358. 


276  NERVOUS    DISEASES 

to  affection  of  the  cranial  nerve  nuclei.  If  the  lesion  extends 
forwards  to  implicate  the  pyramid  of  the  same  side,  there  is 
hemiplegia  of  the  contra-lateral  arm  and  leg. 

Marie's  hereditary  cerebellar  ataxia,  ascribed  to  primary 
parenchymatous  degeneration  of  the  cerebellum  itself,  is  some- 
what similar  to  Friedreich's  ataxia,  but  there  is  no  loss  of  knee- 
jerks  or  affection  of  plantar  reflexes,  scoliosis  does  not  occur,  nor 
pes  cavus,  and  the  age  of  onset  is  somewhat  later.  Optic  atrophy 
is  fairly  common.  Olivo-ponto-cerebellar  atrophy,  described  origin- 
ally by  Dejerine  and  Thomas,  is  a  disease  in  which  there  is  a  primary 
atrophy  of  the  cerebellar  cortex,  the  bulbar  olives,  the  grey  matter 
of  the  pons,  the  middle  cerebellar  peduncles,  and  sometimes  the 
restiform  bodies.  Clinically  there  is  marked  ataxia  or  asynergia 
of  cerebellar  type,  usually  with  nystagmus.  The  disease  does  not 
run  in  families,  and  its  onset  is  in  advanced  life,  usually  after  the 
age  of  sixty. 

Cerebellar  ataxia  also  occurs  in  cerebellar  tumours,  in  vascular 
lesions  of  the  cerebellum,  in  disseminated  sclerosis  affecting  the 
cerebellum  or  its  peduncles,  in  cerebellar  abscess,  in  encephalitis 
of  the  cerebellar  cortex,  an  acute  disease  of  febrile  onset  which  is 
sometimes  met  with  in  children,  and  it  occurs  occasionally  in  old 
age  as  the  result  of  a  primary  senile  atrophy  of  the  cerebellar 
cortex,  especially  affecting  the  Purkinje  cells. ^ 

Cerebellar  ataxia  or  asynergia  differs  in  several  important 
respects  from  the  ataxia  due  to  deficient  sensory  impressions. 
Firstly  there  is  no  impairment  of  joint-sense  nor  of  kinsesthetic 
sense  as  in  the  ordinary  tabetic,  in  fact,  in  pure  cerebellar  disease 
there  is  no  sensory  impairment  whatever.  Again,  cerebellar  ataxia 
is  unaccompanied  by  the  muscular  hypotonia  of  many  cases  of  tabes. 

Rapid  voluntary  movements  in  cerebellar  disease  are,  as  Bab- 
inski  has  pointed  out,  badly  estimated  [mouvements  d&mesurds),  so 
that  the  patient  cannot  arrest  them  at  a  given  point.  Thus 
when  attempting  the  finger-nose  test,  the  patient's  finger  reaches 
his  nose  but  cannot  be  stopped  there  ;  the  movement  continues, 
and  the  finger  pitches  heavily  on  the  nose,  and  may  plunge  past 
it  on  to  the  cheek.  Similarly,  in  the  heel-knee  test,  the  heel  over- 
shoots the  opposite  knee,  landing  above  the  patella.  Again,  if 
the  physician  draws  a  vertical  line  on  a  sheet  of  paper  and  then 
asks  the  patient  to  draw  a  series  of  horizontal  lines  quickly  across 

^  Rossi,  Nouvelle  Iconographie  de  la  Salpetriere,  No.  1,  1907. 


INCO-ORDINATION  277 

the  paper  (say  from  left  to  right),  all  stopping  exactly  at  the  vertical, 
the  cerebellar  patient  overshoots  the  vertical  line.  This  over- 
shooting of  the  mark  in  cerebellar  disease  is  termed  hyper-metria. 
It  is  unaffected  by  closing  the  eyes,  unlike  tabetic  ataxia. 

A  fundamental  character  of  cerebellar  ataxia  is  its  asynergia. 
This  consists  in  a  want  of  synchronism  at  the  different  joints  during 
a  co-ordinated  movement.  Thus,  on  performing  the  heel-knee 
test,  instead  of  the  hip,  knee,  and  ankle  becoming  flexed  simul- 
taneously and  harmoniously,  the  various  joints  move  separately, 
lagging  behind  each  other,  so  that  the  hip  starts  off  with  energetic 
flexion,  whilst  there  is  yet  no  appreciable  flexion  of  the  knee,  the 
distal  part  of  the  limb  remaining  inert ;  then  with  a  second  move- 
ment he  flexes  the  knee.  Cerebellar  asynergia  is  well  seen  in  the 
typical  cerebellar  gait  of  disease  of  the  vermis,  in  which  the  patient, 
although  his  muscular  power  is  unimpaired,  cannot  walk  alone. 
When  supported  on  both  sides,  he  starts  off  with  his  lower  limbs, 
with  the  characteristic  over-action  or  hyper-metria  above  de- 
scribed. Meanwhile  his  trunk,  instead  of  inclining  for\N''ards,  in 
harmony  with  the  advancing  legs,  remains  vertical,  or  even  inchnes 
slightly  backwards,  so  that,  when  the  advancing  lower  limb  reaches 
the  ground,  the  body  as  a  whole  lags  behind  and  tends  to  fall 
backwards,  i.e.  there  is  relative  inertia  of  the  trunk  during  move- 
ment of  the  lower  limbs.  Hence  the  patient  reels  hke  a  drunken 
man,  yet  without  the  stamping  of  the  true  tabetic.  True  cerebellar 
ataxia,  unlike  the  ataxia  of  tabes  dorsaHs,  is  uninfluenced  by  closure 
of  the  eyes. 

A  third  characteristic  of  cerebellar  unsteadiness  is  dys-diadoco- 
Jcinesia.  This  means  the  diminution  or  loss  of  the  power  to 
execute  in  rapid  succession  a  series  of  antagonistic  movements. 
If  we  make  a  patient  perform  a  series  of  rapid  alternate  pronation- 
supination  movements  of  the  forearm,  an  individual  with  cerebellar 
disease  performs  the  action  twice  or  thrice  as  slowly  as  in  health, 
pausing  between  the  two  alternate  movements. 

In  unilateral  cerebellar  disease  we  have  hemi-asynergia  and 
hemi-hyper-metria  of  the  ipso-lateral  limbs,  most  conveniently 
recognised  by  the  heel-knee  test,  whilst  the  dys-diadocokinesia  is 
also  unilateral,  being  confined  to  the  ipso-lateral  upper  limb. 

Less  frequently,  in  pure  cerebellar  disease,  we  meet  with 
intention-tremors  similar  to  those  of  disseminated  sclerosis.  (It 
is,   in    fact,   probable  that    the  intention-tremor  of    disseminated 


278  NERVOUS    DISEASES 

sclerosis  is  of  cerebellar  origin.)  Intention-tremor  is  absent  at 
rest,  and  occurs  only  on  voluntary  movement ;  the  coarseness  of 
its  excursion  depends  on  the  extent  to  which  the  limb  is  outstretched. 
It  is  best  demonstrated  by  making  the  patient  pick  up  or  touch  a 
small  object  at  a  distance  of  an  arm's-length. 

Ataxia  also  occurs  in  some  affections  of  the  higher  cerebral 
centres.  For  example,  there  are  certain  toxic  affections  in  which 
the  patient  becomes  ataxic.  The  most  famihar  variety  is 
that  of  acute  alcoholic  intoxication.  Part  of  this  ataxia  may 
possibly  be  due  to  cerebellar  intoxication,  but  a  large  part  of  it 
is  cerebral,  as  evidenced  by  the  "  mental  ataxia,"  the  disordered 
articulation,  &c.  The  temporary  ataxia  of  fatigue,  of  ^  writer's 
cramp  and  of  other  occupation-neuroses  is  also  probably  ofjcerebral 
origin,  so  also  is  the  transient  ataxia  which  sometimes  follows 
enteric  fever  or  other  exanthemata. 

There  are  certain  diseases  of  the  cerebral  cortex,  in  which  ataxia 
is  distinct.  In  chorea  the  patient  not  only  exhibits  spontaneous 
involuntary  movements,  but  he  also  has  obvious  ataxia  on  volun- 
tary movement.  In  organic  monoflegia,  or  hemiflegia,  especially 
when  slight  in  degree  and  amounting  merely  to  paresis,  obvious 
ataxia  often  exists  in  the  paretic  limbs.  Severe  ataxia  in  the 
contra-lateral  arm  or  leg  is  a  common  sign  in  some  post-Rolandic 
cortical  lesions,  especially  after  bullet-wounds  (see  p.  501).  Hemi- 
ataxia  is  one  of  the  characteristic  phenomena  in  lesions  of  the 
optic  thalamus.  In  such  cases  the  limbs  on  the  side  contra-lateral 
to  the  lesion  are  not  only  ataxic  but  also  partially  anaesthetic  with 
loss  of  join£-sense,  whilst  spontaneous  pains  in  the  affected  limbs 
are  commonly  present.  Sometimes  ataxia  of  the  limbs  precedes  an 
attack  of  hemiplegia — pre-hemiplegic  ataxia,  especially  in  threatened 
softening  from  arterial  thrombosis.  More  often  the  ataxia  appears 
during  convalescence  from  a  slight  hemiplegic  attack  —  fost- 
hemiflegic  ataxia,  when  the  patient  has  to  learn  the  process  of 
co-ordination  again  in  his  paretic  limbs.  This  form  of  ataxia  must 
be  distinguished  from  athetosis,  the  involuntary  slow  writhing 
movements  of  the  limbs  which  occurs  in  old  and  severe  cases  of 
hemiplegia,  especially  of  infantile  hemiplegia. 

Ataxia  is  one  of  the  most  striking  signs  of  disseminated 
sclerosis,  where  the  unsteadiness  of  the  limbs  is  often  associated 
with  a  superadded  coarse  oscillatory  tremor — ^the  so-called  inten- 
tion-tremor.      How  much  of    the    unsteadiness    in    disseminated 


INCO-ORDINATION  279 

sclerosis  is  due  to  cerebral  and  how  much  to  cerebellar  disease  it 
is  difficult  to  say  in  any  individual  case. 

The  tremor  of  hemiplegic  distribution  which  is  observed  in 
the  hmbs  in--  cases  of  lesions  of  the  red  nucleus  or  rubrospinal 
tract  (see  p.  95)  is  present  at  rest,  but  becomes  exaggerated 
on  voluntary  movements,  rendering  them  ataxic.  In  this 
respect  it  contrasts  with  the  tremor  of  paralysis  agitans, 
which  can  usually  be  controlled  to  permit  of  the  perform- 
ance of  a  voluntary  movement. 

Pseudosclerosis  is  a  rare  disease  in  which  many  of  the  clinical 
symptoms  of  disseminated  sclerosis  are  present,  including  the 
staccato  speech,  the  intention-tremors,  and  the  spasticity  of  the 
limbs.  Post  mortem,  however,  no  sclerotic  areas  can  be  detected 
in  the  central  nervous  system.  In  this  disease  there  are  certain 
additional  features  which  help  us  to  recognise  the  condition,  notably 
a  curious  greenish  pigmentation  of  the  corneal  margins,  also 
shrinkage  of  the  liver  and  enlargement  of  the  spleen. ^  Moreover, 
in  pseudo -sclerosis  the  abdominal  reflexes  are  usually  preserved, 
and  the  plantar  responses  are  of  the  normal  flexor  type. 

Finally  we  may  meet  ^vith  ataxia  of  the  most  varied  types 
in  hysteria.  Here  the  affection  is  probably  one  which  impH- 
cates  the  highest  psychical  centres.  The  diagnosis  of  hysterical 
ataxia  rests  on  the  presence  of  other  stigmata  of  hysteria,  to- 
gether with  the  absence  of  evidence  of  organic  disease.  Some- 
times hysterical  ataxia  is  associated  with  "  cortical "  ansesthesia 
of  the  affected  limb.  In  such  a  case  the  patient  may  be  able 
to  move  the  limb  normally  with  her  eyes  open,  but  when  they 
are  closed  ataxia  appears.  This  does  not  necessarily  occur  in 
every  hysterically  anaesthetic  limb,  for  in  many  cases  profound 
anaesthesia  may  be  present  without  ataxia.  The  diagnosis  of 
hysterical  ataxia,  however,  seldom  presents'  much  difficulty  to  a 
careful  observer.  The  disease  which  is  most  often  mistaken  for 
hysteria  is  disseminated  sclerosis  in  its  earlier  stages.  In  both 
diseases  we  may  have  a  history  of  transient  weakness  of  a  limb, 
apparently  clearing  up  completely  for  a  time.  But  in  disseminated 
sclerosis  there  are  objective  evidences  of  organic  disease  in  the 
form  of  pallor  of  the  optic  discs',  nystagmus,  alterations  of  the 
abdominal  and  plantar  reflexes,  sphincter  trouble,  and  so  on. 

1  V.  Striimpell,  Neiirolog.  Centralhlatt,  1913,  p.  1303. 


CHAPTER  XVII 

POSTURES    AND    GAITS 

Postures. — In  health  the  posture  of  the  body  and  of  its  various 
members  is  determined  partly  by  gravity,  partly  by  the  relative 
strength  of  the  muscles  at  the  various  joints.  Therefore, 
inasmuch  as  the  flexor  muscles  of  our  limbs  are  usually  more 
powerful  than  the  extensors,  the  ordinary  posture  of  the  limbs 
at  rest  is  one  of  slight  flexion.  This  is  easily  verified  by 
observing  a  sleeping  child.  In  the  erect  attitude  the  muscles 
of  special  importance  in  maintaining  equilibrium  are  the  ex- 
tensors of  the  hips  and  knees  ;  whilst  in  standing  on  one  foot  the 
peronei  are  of  particular  importance  by  inclining  the  whole  lower 
limb  outwards  from  the  ankle  upwards,  and  bringing  the  centre  of 
gravity  over  the  foot.  The  minor  varieties  of  posture  in  different 
healthy  individuals,  which  we  learn  to  recognise  as  part  of  each 
man's  personal  characteristics,  are  largely  the  result  of  differ- 
ences not  only  in  muscularity  but  of  habit.  The  pose  of  a 
powerful,  muscular  man  is  widely  different  from  that  of  a  thin, 
debilitated  invalid.  Moreover,  if  from  exercise  or  want  of  exercise, 
certain  groups  of  muscles  are  more  or  less  developed  than  the 
normal,  the  posture  is  further  modified,  even  in  health.  For 
example,  we  all  know  the  characteristic  straddling  gait  of  the 
professional  jockey. 

Similar  principles  apply  to  those  cases  of  organic  disease  in 
which  certain  muscles  or  groups  of  muscles  are  affected  by  paralysis. 
Paralysed  limbs  gradually  assume  characteristic  postures,  and  these 
postures  of  organic  disease  are  not  matters  of  haphazard,  but  are 
determined  by  anatomical  rules. 

If  the  muscular  paralysis  be  the  result  of  a  lower  motor 
neurone  lesion,  in  the  anterior  cornua,  anterior  nerve-roots,  nerve 
trunks  or  muscle-fibres,  the  paralysed  muscles  become  wasted. 

Sometimes  the  affected  muscles  undergo  cicatricial  contrac- 
tion, and  thereby  fix  the  part  in  an  abnormal  posture.  This 
is  what  occurs  in  ischsemic  myositis,  to  which  we  have  already 
referred  (p.  248).     It  also  occurs  in  fixed  or  congenital  torticollis 

280 


POSTURES    AND    GAITS 


281 


(which  must  not  be  confounded  with  spasmodic  torticollis,  de- 
scribed on  p.  101).  Congenital  torticollis  is  due  to  shortening  of 
one  sternomastoid,  resulting  from  an  injury  to  the  muscle  during 
birth.  The  head  deviates  slightly  to  one  side  and  cannot  be  turned, 
either  actively  or  passively,   towards  the  side  of  the  shortened 


I 


Fig.  124.— Chronic  myelitis  of  fifth  cervical  segment,  with  atrophic 
paralysis  of  deltoid,  biceps  and  supinators. 

sternomastoid.     Unlike  spasmodic  torticollis,  it  is  unaccompanied 
by  active  muscular  spasm. 

More  commonly,  in  a  case  of  lower  motor  neurone  palsy,  the 
unopposed  non-paralysed  antagonists  slowly  become  contracted, 
and  fix  the  limb  in  a  certain  definite  posture  which  is  best  demon- 
strated if  the  patient  tries  to  throw  the  paralysed  muscles  into 
action,  in  which  case  the  antagonists  contract  alone. 


282  NERVOUS    DISEASES 

For  example,  Fig.  124  is  a  photograph  of  a  woman  who  had 
a  locahsed  lesion  in  the  anterior  cornua  of  the  cord  at  the  level 
of  the  fifth  cervical  segment.  Amongst  the  chief  muscles  supplied 
by  the  anterior  cornua  at  that  level  are  the  deltoid,  biceps  and 
supinators.  These  muscles  underwent  atrophy  and  their  unopposed 
antagonists  became  contracted.  As  a  result  we  see  that  from 
paralysis  of  the  deltoid  and  contraction  of  its  opponents  the  shoulder 


Fig.  125. — Paralysis  of  external  popliteal  nerve  of  right  leg,  the  result 
of  a  bullet-wound.     Showing  muscular  atrophy  and  drop-foot. 

is  adducted,  similarly  from  paralysis  of  the  biceps  the  elbow  is 
extended  by  its  opponents,  and  from  paralysis  of  the  supinators 
the  forearm  is  hyperpronated  by  their  antagonists.  This  posture  is 
characteristic  of  a  cord  lesion  at  the  fifth  cervical  segment. 

Fig.  125  shows  the  posture  assumed  in  a  case  of  paralysis  of  the 
external  popliteal  nerve.  This  nerve  was  divided  by  a  bullet- 
wound  in  an  officer's  right  leg.  In  addition  to  anaesthesia  corre- 
sponding to  the  cutaneous  distribution  of  the  nerve,  the  figure 
shows  the  presence  of  foot-drop  due  to  paralysis  of  the  anterior  tibial 


POSTUKES    AND    GAITS 


283 


group  of  muscles,  with  unopposed  contraction  of  the  calf  muscles. 
Here,  of  course,  the  action  of  gravity  is  a  factor  as  well,  for  the 
weight  of  the  foot  tends  to  increase  the  foot-drop. 

Fig.  127  shows  the  posture  in  a  case  of  paralysis  of  the 
musculo-spiral  nerve.  The  patient  is  trying  to  extend  both  his 
wrists.  On  the  paralysed  side  we  notice  the  atrophy  of  the 
supinator  longus  and  the  paralysis  of  the  extensors  of  the  wrist 


Fia.  126. — Case  of  claw-hand  from  rupture  of  first  thoracic  root,  fol- 
lowing a  dislocation  of  the  right  shoulder.  Note  the  atrophy  of 
intrinsic  muscles  of  the  right  hand  ;  also  the  pseudo-ptosis  on 
that  side,  due  to  affection  of  cervical  sympathetic. 

and  fingers,  also  the  characteristic  swelHng  on  the  dorsum  of  the 
hand,  probably  bursal  in  origin,  which  appears  in  long-standing 
cases  of  drop-wrist. 

Lower  motor  neurone  lesions  affecting  the  muscles  of  the  hand 
produce  certain  highly  characteristic  postures  : — 

(1)  The  so-called  monkey-hand  (main  de  singe),  in  which 
there  is  a  localised  wasting  of  the  thenar  muscles  with  loss  of  the 
power  of  opposing  the  thumb. 

(2)  Claw-hand,  or  main  en  griffe,  due  to  paralysis  of  the  inter- 
ossei  and  lumbricales,  in  which  the  fingers  are  now  controlled  by 


284 


NERVOUS    DISEASES 


tlie  long  flexors  and  extensors  alone.  In  this  condition  the 
proximal  phalanges  become  hyper-extended,  whilst  the  two  distal 
phalanges  are  flexed  in  a  hook-like  fashion.  Meanwhile  the  power 
of  abducting  the  fingers  by  the  interossei  is  lost.  When  the  ulnar 
nerve  alone  is  paralysed  the  deformity  is  more  marked  in  the  two 
ulnar  fingers,  since  the  lumbricales  corresponding  to  the  index 
and  middle  fingers  (supplied  by  the  median  nerve)  escape. 

(3)   The    preacher's    hand    [main     de    prMicateicr) ,    specially 
common  in  syringomyelia.     In  this  variety,  from  survival  of  the 


Fig-.  127. — -Left-sided  musculo-spiral  paralysis.     Showing  drop-wrist 
and  atrophy  of  supinator  longus. 

long  extensors,  the  hand  is  extended  or  even  hyper-extended,  at 
the  wrist. 

The  loss  of  the  movements  of  adduction  and  abduction  in 
the  extended  fingers,  due  to  interosseal  paralysis,  develops  when 
the  "main  de  singe"  becomes  the  ^' main  en  griff e."  As  a 
matter  of  fact,  these  three  positions  of  the  hand  occur  in  lesions 
not  only  of  the  anterior  cornua  (as  in  progressive  muscular 
atrophy,  syringomyeha,  amyotrophic  lateral  sclerosis),  but  also  in 
anterior  radicular  lesions,  in  lesions  of  the  lower  roots  of  the 
brachial  plexus  (see  Fig.  126),  in  toxic  or  infective  neuritis,  in 
leprosy,  in  family  neuritic  diseases  like  peroneal  muscular  atrophy 
and  progressive  hypertrophic  neuritis. 

If    the    paralysis    be   due   to  an  upper  motor  neurone  lesion, 


POSTURES    AND    GAITS  285 

the  law  which  determines  the  posture  is  different.  We  no 
longer  have  atrophic  paralysis,  limited  to  a  particular  muscle  or 
muscles  as  in  a  lower  motor  neurone  lesion.  Instead,  there 
gradually  develops  a  spastic  paralysis,  in  which  all  the  muscles 
of  the  affected  limb  or  segment  of  a  limb  are  more  or  less  paralysed 
and  in  a  state  of  hyper-tonus. 


Fig.  12S.  Fig.  128a. 

Case  of  left-sided  infantile  hemiplegia  in  a  patient  aged  7  years.  Onset 
of  hemiplegia  Ave  years  previously.  Showing  posture  of  limbs.  In 
Fig.  128  note  athetosis  of  left  fingers.  In  Fig.  128A  note  inversion 
of  ankle  and  drawing  up  of  heel. 

The  condition  is  best  studied  in  the  lower  limbs.  There  are  two 
distinct  types  of  spastic  paralysis,  described  by  Babinski  as 
"  paralysis  in  extension  "  and  "  paralysis  in  flexion  "  respectively. 
The  essential  difference  between  these  two  types,  as  Walshe  has 
shown,  1  is  that  in  the  "  extended  "  form  of  spastic  paralysis  both 
extensor  and  flexor  groups  of  muscles  are  in  a  state  of  exalted 

1   Brain,  1914,  vol.  xxxvii.  pp.  269-336. 


286  NERVOUS    DISEASES 

reflex  activity,  whereas  in  the  "  flexed  "  type,  only  the  flexor  group 
of  muscles  retains  this,  the  extensors  showing  diminished  or  absent 
reflex  action. 

The  extended  type  of  s'pastic  jmralysis  only  occurs  in  pure 
pyramidal  affections,  as  in  ordinary  hemiplegia  and  in  pure  lateral 
sclerosis  of  the  spinal  cord.  Thus  in  a  chronic  hemiplegia  the 
famihar  posture  of  the  upper  Hmb  is  that  of  flexion  with  pronation, 
that  of  the  lower  limb  being  one  of  slight  extension  at  the  hip 
and  knee,  with  plantar  flexion  and  inversion  of  the  ankle,  and  a 
tendency  to  dorsiflexion  of  the  toes  (see  Figs.  128  and  128a),  the 
limb  as  a  whole  thus  becoming  outstretched  or  lengthened.     In 


FiC4.  129. — Transverse  softening  of  the  spiral  cord,  producing 
spastic  paraplegia  of  flexed  type. 

the  spastic  hmbs  all  the  deep  reflexes  are  increased,  and  there  is 
a  Babinski  plantar  response  on  stimulation  of  the  sole. 

iThe  flexed  type  of  spastic  paraplegia  (see  Fig.  129)  occurs  only 
in  diffuse  spinal  lesions,  never  in  pure  pyramidal  disease.  The 
posture  of  the  lower  Hmb  is  one  of  flexion  of  the  hip  and  knee, 
with  dorsiflexion  of  the  ankle,  the  whole  limb  being  puUed  up  or 
shortened.  In  this  type  of  contracture  the  knee-jerks  and  ankle- 
jerks  are  feeble  or  absent,  and  there  is  no  ankle-clonus.  Neverthe- 
less the  hamstring- jerks  are  found  to  be  excessively  brisk.  Fre- 
quent involuntary  flexor  spasms  occur  in  the  paralysed  Hmb, 
temporarily  exaggerating  its  flexed  posture.  The  Babinski  plantar 
response  is  present.  To  produce  this  flexed  type  of  spastic  para- 
plegia, the  interruption  of  some  other  afferent  tract,  in  addition 
to  the  pyramidal  tract,  is  essential  (see  "  sub-cortico-spinal  tracts," 


POSTURES    AND    GAITS  287 

pp.  12-14).  The  effect  of  such  a  lesion  in  the  extra-pyramidal  motor 
path  is  to  aboUsh  the  reflex  tonus  in  the  paralysed  extensor  muscles 
without  affecting  the  reflex  activity  of  the  paralysed  flexor  group. 

The  spastic  posture  in  hemiplegia  does  not  come  on  at  once. 
There  is  an  initial  flaccid  stage,  lasting  several  weeks  or  even 
months,  before  the  spastic  rigidity  sets  in.  (In  a  small  number 
of  cases  the  hemiplegia  may  remain  permanently  flaccid.)  But 
even  during  this  flaccid  stage  the  postures  of  the  hemiplegic  limbs 
are  often  different  from  those  of  the  unaffected  side  at  rest.  One 
of  the  most  characteristic  signs  is  an  apparent  broadening  of  the 
lower  limb  (Heilbronner's  ^  "  hreites  Bern  ").  This  consists  in  an 
outward  rotation  of  the  lower  hmb  at  the  hip-joint,  due  to  its 
own  weight  when  in  the  recumbent  posture  (analogous  to  the 
displacement  which  occurs  in  fracture  of  the  neck  of  the  femur). 
The  thigh,  therefore,  when  looked  at  from  the  front,  appears  broader 
than  on  the  healthy  side.  Moreover,  the  flaccid  paralysed  muscles 
fall  back  by  their  own  weight,  and  on  transverse  section  the  thigh 
forms  a  flattened  oval  instead  of  an  approximate  circle  as  on  the 
healthy  side.  This  apparent  broadening  of  the  paralysed  thigh  can 
be  well  seen  if  the  patient  be  seated  on  a  hard,  flat  seat.  It  does 
not  occur  in  hysterical  hemiplegia. 

In  functional  paralysis  the  conditions  are  different.  Hysteria, 
it  is  often  said,  may  simulate  organic  disease — thus  we  may  have 
functional  hemiplegia,  paraplegia,  or  monoplegia.  But  if  we 
examine  carefully  we  usually  find  that  this  similarity  is  more  or 
less  rough  and  inaccurate.  And  why  ?  Because  hysterical  con- 
tractures are  not  governed  by  anatomical  rules  ensuring  the  x^re- 
ponderance  of  the  stronger  muscles.  Hysterical  contractures 
usually  present  some  points  in  which  they  differ  from  the  postures 
of  genuine  organic  lesions.  Thus,  for  example,  we  do  not  have 
loss  of  deep  reflexes  nor  muscular  atrophy  with  R.D.  as  in 
lower  motor  neurone  lesions  ;  nor  do  we  have  an  extensor  plantar 
reflex  nor  a  true  clonus  as  in  genuine  pyramidal  disease.  More- 
over, if  hysterical  hemiplegia  affects  the  face  we  have,  not  a 
true  paralysis,  but  a  glosso-labial  hemispasm.  Figs.  130  and 
131  are  from  a  case  of  functional  hemiplegia,  in  which  the 
contracture  alone  was  enough  to  distinguish  it  from  an  organic 
case.  Instead  of  the  usual  flexed  and  pronated  postm-e  of  the 
upper  hmb,  we  observe  that  the  elbow  and  wrist  are  extended, 

'  Deutsche  Zeitachrift  fur  Nervenheilhunde,  Bd.  28,  1904,  s.  1. 


288 


NERVOUS   DISEASES 


the  forearm  is  supinated,  and  the  fingers  are  half-bent  in  a  hook- 
like fashion,  whilst  in  the  lower  limb  the  inversion  of  the  ankle 
is  overdone,  out  of  all  proportion  to  the  ordinary  equinus  position. 


Fig.  130. 


Fig.  131. 


From  a  case  of  right-sided  hysterical  hemiplegia  in  a  left-handed  patient. 
Showing  contractures  of  hand  and  foot.  The  right  forearm  was 
rigidly  supinated,  but  is  being  passively  semi-pronated  by  the 
physician,  to  show  the  posture  of  the  hand. 

The  contracture  in  this  patient  appeared  suddenly,  as  is  so  often 
the  case  in  hysteria,  unlike  the  gradual  development  of  an 
organic   contracture.     Fig.   132   shows  a  peculiar  contracture   of 


Fig.  132. — Functional  paraplegia.     Showing  longitudinal  fold  of  soles. 


the  soles  in  another  case  of  hysterical  paraplegia,  in  which  the 
feet  had  a  fold  running  longitudinally  along  the  soles,  totally 
unlike  any  organic  contracture. 


POSTURES    AND    GAITS 


289 


Fig.  133  shows  a  case  of  left-sided  hysterical  hemiplegia,  in 
which  the  contracture  of  the  upper  limb  differs  from  that  of 
organic  disease  ;  for  wliilst  the  shoulder,  elbow  and  wrist  are  rigid, 
the  fingers  are  flaccid — a  combination  which  does  not  occur  in 
organic  hemiplegia.    We  also  observe  that  this  patient  has  glosso- 


FiG.  133. — Left-sided  hysterical  hemiplegia  with  glosso-labial  spasm 
on  protrusion  of  tongue.  The  left  upper  limb  was  also  rigidly  con- 
tracted at  the  shoulder  and  elbow,  the  hand  being  flaccid. 


labial  hemispasm.  When  she  protrudes  her  tongue  it  deviates 
considerably  to  the  paralysed  side,  but  in  such  an  exaggerated 
fashion  that  it  is  easy  to  recognise  the  deformity  as  spasmodic, 
not  paralytic.  We  also  note  that,  when  the  tongue  is  protruded, 
the  face  on  the  paralysed  side  goes  into  a  state  of  spasm,  so  that 
the  left  naso-labial  fold  is  deeper  than  on  the  healthy  side,  a 
condition  which  is  the  reverse  of  what  we  find  in  organic  hemi- 

T 


290 


NERVOUS    DISEASES 


plegia.      Glosso-labial  hemispasm  such  as  this  is  not   a  common 
sign,  but  when  it  occurs  it  is  pathognomonic  of  hysteria. 

Hysterical  contractures  often,  but  not  always,  disappear  during 
sleep  or  during  deep  anaesthesia.  If  the  contracture  has  persisted 
for  months,  adhesions  may  form  in  the  joints,  so  that  even  under 
an  anaesthetic  the  contracture  may  not 
completely  relax,  and  we  may  have  to 
break  down  the  adhesions  forcibly. 

The  postures  of  organic  paralyses, 
then,  whether  supra-  or  infra-nuclear, 
are  definite  and  comparatively  simple, 
being  governed  by  the  anatomical  rules 
we  have  mentioned.  Hysterical  postures, 
on  the  other  hand,  being  under  no  such 
restrictions,  may  assume  the  most  varied 
and  weird  appearances,  examples  of  which 
might  be  multiplied  indefinitely.  Whether 
spastic  or  paralytic,  the  motor  pheno- 
mena of  hysteria  are  usually  "  sy  sterna - 
tised."  As  Babinski  has  pointed  out, 
they  merely  affect  one  or  more  "  sys- 
tems "  of  voluntary  movements  which 
the  muscles  of  the  face  or  of  a  hmb 
are  caUed  on  to  perform.  Hysterical 
postures  are  caricatures  or  exaggerations 
of  some  spastic  or  paralytic  posture, 
which,  however,  never  corresponds  in 
distribution  to  a  peripheral  nerve  nor 
Hyper-extension  of  ^^  ^  Spinal  Segment  but  to  Some 
well-recognised  attitude.  Therefore  a 
hysterical  paralysis  or  a  hysterical  con- 
tracture can  always  be  imitated,  whereas  an  organic  contracture 
is  never  accurately  imitated  by  a  hysterical  patient. 

In  many  cases  of  tabes  dorsalis  there  is  marked  deficiency  of 
muscular  tonus,  a  condition  known  as  hypotonia.  This  slackness  of 
the  muscles  has  a  remarkable  influence  on  the  patient's  postures. 
Thus,  for  example,  hypotonia  of  the  peronei  increases  the  difficulty 
of  standing,  since  whenever  the  patient  lifts  one  leg,  the  other 
fixed  leg  is  no  longer  pulled  outwards  as  in  health  to  bring  the 
centre  of  gravity  over  the  fixed  foot.     When  the  hamstrings  and 


Fig. 134 

knees  in  a  case  of  tabes 
"genu  recurvatum." 


POSTURES    AND    GAITS 


291 


sural  muscles  behind  the  knee  are  hypotonic  (see  Fig.  134),  the 
joint  becomes  hyper- extended  in  the  erect  posture — the  so-called 
"  genu  recurvatum  " — unlike  the  knee-joint  of  a  healthy  individual, 
in  which,  however  strongly  the  knee  be  extended,  there  always  re- 
mains a  concavity  behind.  This  hypotonia  of  the  popliteal  muscles 
produces  another  very  characteristic  sign  of  tabes,  which  is 
that  when  the  patient  lies  in  bed  with  the  knee  extended,  the 
heel  can  be  passively  raised  whilst  the  back  of  the  knee  re- 
mains in   contact  with   the  bed    (see   Fig.    135).     Hypotonia   of 


Fig.  loo. — Tabetic  liypotunia  (if  popliteal  iiiuseles. 

the  muscles  of  the  trunk  and  lower  limbs,  in  tabes,  may  permit 
of  the  patient  assuming  the  most  extraordinary  postures  without 
pain — postures  which  are  impossible  to  any  ordinary  individual 
who  is  not  a  professionally  trained  contortionist  (see  Figs.  136, 
137  and  138). 

Amyotonia  congenita  (sometimes,  though  less  aptly,  called 
myatonia  congenita)  is  a  condition  of  extreme  flaccidity  of  the 
muscles,  which  are  soft  and  lax  on  palpation.  When  thrown  into 
voluntary  contraction  they  do  not  harden  like  ordinary  muscles, 
and  it  may  be  impossible  by  palpation  to  distinguish  them  from 
the  subcutaneous  tissues.  The  joints  are  flail-like,  and  can  be 
placed  in  all  sorts  of  fantastic  postures  (see  Fig.  139).     There  is  no 


292  NERVOUS    DISEASES 

true  motor  paralysis,  although  voluntary  movements  are  devoid 
of  vigour.  The  amyotonia  is  most  marked  in  the  lower  limbs. 
The    sphincters    are     unaffected.       The    electric    excitability    is 


Fig.  136. — Tabetic  hypotonia  of  gluteal  and  hamstring  muscles. 

diminished  both  to  faiadism  and  to  galvanism,  but  without 
polar  changes.  The  child  can  bear  strong  faradic  stimulation 
with  unusual  stoicism.     The  deep  reflexes  are  absent,  whilst  the 


Fig.  137. — Tabetic  hypotonia  of  muscles  of  lower  limbs  and  trunk. 

cutaneous  and  organic  reflexes  are  normal.  The  condition, 
which  is  congenita],  is  really  a  variety  of  myopathy.  The  phe- 
nomena are  usually  detected  within  the  first  twelve  months 
after  birth.     Sometimes  the  symptoms  improve,  and    the   deep 


POSTURES    AND    GAITS  293 

reflexes  may  even  return,  but  the  patient  never  attains  normal 
muscular  power.  Pathologically  the  muscles  show  changes 
identical  with  those  found  in  primary  myopathy. 


Fig.  138. — Tabetic  hypotonia  of  adductor  muscles. 

Gaits. — Unlike  some  of  the  lower  animals — for  example,  the 
chicken  or  the  lamb — the  human  infant  at  birth  cannot  stand  or 
walk.     It  is  not  until  the  child  reaches  the  age  of  about  eighteen 


Fig.  139. — Amyotonia  congenita  in  a  child  of  2^  years, 
showing  inability  to  sit  up. 

months  that  he  begins  to  walk.  First  he  learns  to  stand,  and  then 
after  repeated  efforts  he  succeeds  in  walking.  During  the  process 
of  learning,  he  reels  and  falls  about  just  like  an  adult  with  cerebellar 
disease. 


294  NERVOUS    DISEASES 

We  do  not  all  of  us  walk  exactly  in  the  same  fashion.  Even 
healthy  individuals  show  minor  differences  in  gait.  An  old  man 
walks  differently  from  a  youth,  a  soldier  differently  from  a 
sailor,  and  a  woman  advanced  in  pregnancy  differently  from  a 
maiden.  The  wearing  of  ordinary  boots  with  artificial  heels 
also  modifies  the  -gait,  so  that  in  health  the  first  part  of  the 
boot  to  show  signs  of  wear  is  usually  the  back  of  the  heel  on  the 
outer  side.  Ladies'  high-heeled  boots  modify  the  gait  still  more, 
throwing  the  weight  of  the  body  unduly  forwards  towards  the 
heads  of  the  metatarsal  bones. 

When  testing  the  gait  in  cases  of  nervous  disease  it  is  advisable 
to  have  the  patient's  lower  limbs  well  exposed,  and  without  boots. 
To  get  a  good  view  of  the  limbs  it  is  well  to  have  a  minimum 
of  clothing  on  the  patient.  A  good  plan  is  to  have  him 
clad  in  some  light  garment  like  a  shirt,  whose  tail  is  pulled  for- 
wards between  the  legs  from  behind  and  pinned  in  front,  thereby 
leaving  the  upper  limbs  free.  We  ask  the  patient  to  walk  straight 
away  from  us  towards  some  given  point,  then  to  turn  round  and 
come  back. 

In  a  normal  gait  the  limbs  are  moved  forward  easily,  the  feet 
neither  scraping  the  ground  whilst  being  lifted,  nor  being  unduly 
stamped  down  as  they  descend.  The  forward- moving  or  "  active  " 
leg  is  the  one  which  carries  the  weight  of  the  body.  The  trunk  and 
pelvis  therefore  lean  a  Httle  towards  the  corresponding  side  during 
the  "  active  "  phase  of  each  Umb.  This  trunk  movement  is  attained 
partly  by  the  action  of  the  gluteal  muscles,  partly  by  the  sacro- 
lumbar  muscles  of  the  same  side.  A  short,  thick-set  person  with 
a  broad  pelvis  tends  to  have  a  "  waddHng  "  gait,  as  the  weight 
of  his  trunk  is  shifted  across  from  one  side  to  the  other. 
When  the  gluteal  muscles  are  weak,  the  patient  waddles 
excessively,  in  his  efforts  to  throw  his  weight  to  each  side 
alternately. 

The  gait  is  altered  in  various  diseases.  Thus  it  may  become 
spastic,  ataxic,  reehng,  high-stepping,  and  so  on. 

A  spastic  gait  occurs  in  lesions  of  the  pyramidal  tract — for 
example,  in  hemiplegia,  in  diplegia,  and  in  spastic  paraplegia.  In 
organic  hemiplegia  the  active  forward-projection  of  the  Umb  is 
especially  difficult  on  the  paralysed  side,  and  the  weight  of  the  body 
has  to  be  carried  forwards  by  the  aid  of  the  other  side  plus 
gravity,  unlike  the  normal  gait  in  which  the  weight  is  carried  entirely 


POSTURES   AND    GAITS  295 

by  the  "  active  "  advancing  leg.  Thus  when  the  hemiplegic  leg 
ought  to  be  in  the  "  active  "  phase,  it  is  not  properly  flexed  at 
the  knee  or  ankle,  nor  is  it  actively  pushed  forwards  but  merely 
dangles  forward  like  a  pendulum, 'not  directly  forwards,  but  swing- 
ing in  a  circular  fashion  round  the   opposite  hip   as  on  a  pivot. 


Fig.  140. — Spastic  diplegia.     Showing  "  scissor-gait  "  and 
conjugate  automatic  movements  of  the  upper  limbs. 

When  the  "  active  "  phase  of  the  non-paralysed  limb  occurs,  the 
hemiplegic  foot  (owing  to  weakness  of  the  peronei  and  dorsifiexors 
of  the  ankle,  with  over-action  of  the  inverters  and  calf  muscles) 
stays  on  the  ground  too  long,  thereby  scraping  the  front  part  of 
the  foot,  especially  the  ball  of  the  great  toe ;  the  stride  of  the 
paralysed  limb  is  therefore  shorter  than  on  the  healthy  side.  In  a 
case  of  spastic  diplegia,  or  double  hemiplegia,  the  patient  is  unable 
to  project  either  leg  forwards  in  the  ordinary  way,  but  has  to  jerk 


296 


NERVOUS   DISEASES 


each  forwards  in  turn  with  a  circular  swing,  so  that,  in  a  well- 
marked  case,  not  only  does  the  patient  take  abnormally  short  steps, 
catching  the  ball  of  each  foot  on  the  ground,  but  from  the  circular 
swing  of  the  limbs,  together  with  their  adductor  spasm,  they  cross 
alternately  in  front  of  each  other,  producing  the  cross-legged  or 
"scissor  "  gait  (see  Fig.  140).  Meanwhile  the  trunk  and  upper  limbs 
make  violent  jerky  movements,  swinging  the  body  from  one  side  to 
the  other.  A  milder  degree  of  diplegic  gait  often  occurs  in  old 
people  who  have  had  attacks  of  lacunar  hemiflegia  on  both  sides 


Fig.  141. — Gait  in  a  case  of  left-sided  hysterical  hemiplegia.     The  marks 
on  the  left  leg  are  scars  of  self-iniiicted  burns. 

of  the  brain.  In  such  cases  the  gait  shows  an  abnormal  shortening 
of  the  stride  ('"  marche  a  petits  pas  ")  without  actual  scissor-gait. 
In  ordinary  spastic  paraplegia  from  cord  disease,  there  is  not  the 
cross-legged  gait  of  diplegia,  but  the  patient  moves  stiffly  along, 
taking  abnormally  short  steps,  the  front  part  of  the  feet  clinging 
to  the  ground,  thus  wearing  out  the  toes  of  the  boots.  Meanwhile 
the  tendency  to  ankle-clonus  causes  a  "  trepidation  "  of  the  whole 
body  in  severe  cases,  from  tremor  of  the  feet.  Such  a  patient 
stumbles  over  the  slightest  obstacles. 

The  gaits  of  hysteria  are  of  the  most  varied  types.     For  example, 
in  hysterical  hemiplegia,  the  patient  often  pushes  the  paralysed 


POSTURES    AND    GAITS 


297 


foot  along  the  ground  as  if  on  a  skate,  or  drags  it  helplessly  along 
with  its  dorsum  resting  on  the  ground,  as  seen  in  Fig.  141. 
If  this  is  bilateral,  the  patient  is  totally  unable  to  walk  or 
stand.  Or  the  foot  may  be  held  in  a  position  of  talipes 
calcaneus,  or  the  patient  may  walk  on  the  outer  border  of  the 
foot  (sec  Fig.  142)  when  walking,  even  when  no  such  posture  is 
present  at  rest ;  or  one  lower  limb  may  be  acutely  flexed  at  the 
hip  and  knee,  so  that  the  patient  has  to  use  crutches. 

Or    again,   the   patient   may  have  a  zig-zag  gait,  or  he  may 


Fig.  142. — Gait  in  a  case  of  hysterical  monoplegia  of  right  leg. 

throw  one  leg  about  with  a  wild  flourish  before  bringing  it  to  the 
ground,  or  may  suddenly  kneel  down  every  few  steps — these  are 
tics  of  gait.  Astasia-ahasia  is  the  term  applied  to  a  condition  in 
which  a  hysterical  patient  is  unable  to  stand  or  walk,  although 
capable  in  the  recumbent  posture  of  performing  all  movements  of 
the  lower  limbs  normally.  The  varieties  of  hysterical  gaits  are 
practically  unHmited,  but  every  one  of  them  differs  in  some 
respect  from  the  gait  of  organic  disease. 

The  side-gait  (Schiiller's  "  Flankengang  ")  is  a  useful  means  of 
diagnosing  between  organic  and  hysterical  hemiplegia.  To  test  it, 
the  patient  is  placed  on  a  line  and  made  to  move  along  it  side- 
ways in  a  given  definite  direction — say,  towards  the  right.  A 
normal  individual  during  this  movement,  first  leans  his  trunk  to 


298  NERVOUS    DISEASES 

the  left,  then  balancing  his  weight  on  the  left  leg,  he  lifts  the 
right  from  the  ground,  abducts  it  by  a  muscular  effort,  brings  the 
trunk  erect  again,  puts  down  the  right  foot,  last  of  all  lifting  the 
left  leg,  adducting  it  and  placing  it  alongside  the  right.  How  is 
this  performed  in  organic  hemiplegia  ?  We  find  that  the  hemi- 
plegic  patient  moves  sideways  towards  the  paralysed  side  well, 
but  badly  towards  the  healthy  side,  so  that  in  right-sided  hemi- 
plegia the  patient,  when  going  sideways  towards  the  right  moves 
normally,  but  when  going  towards  the  left  he  drags  his  right 
leg  in  the  movement  of  adduction.  This  difference  in  the  side- 
gait  on  the  two  sides  in  organic  hemiplegia  is  often  quite  evident 
when  the  forward  gait  shows  very  little  abnormality.  To  show 
the  phenomenon  properly,  the  patient  must  not  be  too  severely 
paralysed  to  stand  or  walk,  nor  must  he  have  shortening  of  the 
limb,  as  in  old  infantile  hemiplegia.  These  two  exceptions,  how- 
ever, are  readily  recognised  by  other  signs.  In  hysterical  hemi- 
plegia the  side-gait  is  impaired  on  both  sides,  not  merely  on 
the  healthy  side. 

An  ataxic  gait  is  seen  most  typically  in  tabes  dorsalis ;  but  it 
occurs  also  to  a  lesser  degree  in  other  diseases  imphcating  the 
posterior  columns  of  the  cord — for  example,  in  Friedreich's  ataxia, 
in  chronic  meningo-myelitis,  or  in  tumours  of  the  posterior  columns, 
also  in  ataxic  paraplegia  or  postero -lateral  sclerosis,  whether  due 
to  disseminated  sclerosis  or  to  other  causes.  Of  all  these,  the 
tabetic  gait  is  the  most  characteristic.  In  this  there  is  no  motor 
weakness  of  the  limbs,  but  they  are  characteristically  unsteady. 
The  patient  walks  on  too  broad  a  base,  with  his  legs  unduly  wide 
apart.  He  lifts  them  suddenly  and  violently,  raising  them  too  high, 
then  bangs  them  down  forcibly  in  flail-like  fashion,  stamping  the 
heels  on  the  ground.  He  tries  to  guide  his  tottering  course  by 
watching  the  ground.  Therefore  if  his  eyes  be  shut,  or  if  he 
be  in  the  dark,  and  especially  if  he  narrows  his  base  by  placing 
the  feet  close  together,  he  tends  to  fall.  In  slight  cases  of  tabetic 
ataxia,  when  the  patient  is  in  this  position,  he  may  not  actually 
fall,  but  we  can  see  the  tendons  on  the  dorsum  of  the  feet  actively 
in  movement,  in  the  effort  to  preserve  the  balance.  With  this  gait 
we  usually  have  absence  of  the  knee-  and  ankle- jerks,  Argyll- 
Robertson  pupils,  and  various  other  signs,  such  as  lightning  pains, 
ansesthesiae,  crises,  and  lymphocytosis  of  the  cerebro- spinal  fluid.  In 
Friedreich's  ataxia  the  patient  is  commonly  an   adolescent,   and 


POSTURES    AND    GAITS  299 

though  the  knee-  and  ankle-jerks  are  absent,  as  in  tabes,  the  pupils 
react  normally,  there  are  no  lightning  pains  nor  crises,  and  we 
usually  find  nystagmus,  scoliosis,  pes  cavus,  and  a  peculiar  affec- 
tion of  articulation.  In  ataxic  paraplegia  or  postero-lateral  sclerosis, 
where  the  lateral  columns  are  implicated  as  well  as  the  posterior, 
the  patient  is  ataxic,  but  witli  increased  knee-jerks,  possibly 
ankle-clonus,  and  usually  an  extensor  type  of  plantar  reflex. 


Fig.  143. — Case  of  right-sided  extra-cerebellar  tumour  arising 
from  sheath  of  auditory  nerve. 

A  reeling  or  titubating  gait  is  one  of  the  commonest  signs  of 
cerebellar  disease,  although  it  is  also  met  with  in  severe  vertigo 
of  any  variety,  whether  from  alcoholic  intoxication,  from  ear 
disease,  from  diplopia,  or  other  cause.  In  cerebellar  disease  the 
patient  staggers  along,  with  an  occasional  sudden  lurch  to  one 
or  other  side,  but  neither  lifting  his  feet  too  high  nor  stamping 
them  down,  as  in  tabes.  Not  uncommonly  the  cerebellar  patient 
has  a  tendency  to  stagger  persistently  in  some  particular  direction, 
depending  on  the  position  of  the  cerebellar  lesion— thus  he  may 
tend  to  fall  forwards,  backwards,  or  to  one  side.  As  a  rule,  he 
manages  to  pull  himself  up  after  he  has  deviated  one  or  two  steps 
from  his  straight  course.    In  some  cases  of  unilateral  tumour  of  the 


300 


NERVOUS    DISEASES 


cerebellum,  in  the  region  of  the  vestibular  nerve,  the  posture  of 
the  head  is  altered,  the  ear  being  tilted  towards  the  shoulder  on 
the  side  opposite  to  the  lesion,  and  the  face  turned  slightly  in  the 
reverse  direction,  i.e.  towards  the  side  of  the  lesion.  This  is  well 
seen  in  Fig.  143,  which  represents  a  woman 
who  had  a  tumour  originating  from  the 
meninges  over  the  right  petrous  bone,  and 
invading  the  right  lateral  lobe  of  the  cere- 
bellum. This  growth  was  successfully  local- 
ised and  removed,  but  the  patient  unfor- 
tunately died  shortly  after.  This  "  vesti- 
bular  attitude,"  however,  although  common 
in  lateral  tumours,  is  not  constant  in  its 
direction.  For  example,  cases  have  been 
recorded  in  which  the  lateral  tilting  of  the 
head  was  towards  the  side  of  the  lesion, 
and  the  rotation  of  the  face  to  the  opposite 
side. 

A  high- stepping  gait  occurs  in  patients 
who  have  foot-drop.  Such  a  patient,  to 
clear  his  foot  from  the  ground,  hfts  the 
leg  too  high,  flinging  the  ankle  up  as  it 
were,  instead  of  actively  dorsiflexing  it. 
This  gait  occurs  typically  in  peripheral 
neuritis,  also  in  muscular  dystrophies,  and 
occasionally  in  lesions  of  the  cauda  equina 
or  lower  part  of  the  lumbosacral  region  of 
the  spinal  cord.  It  also  occurs  unilaterally 
in  paralysis  of  the  external  popliteal  nerve. 
The  gait  and  posture  of  muscular  dystrophy 
also  possess  other  characteristic  features. 
Thus  from  weakness  of  the  gluteal  muscles 
the  patient,  in  the  erect  posture,  arches  his  back,  in  order  to  keep 
the  hips  extended  (see  Fig.  144) ;  this  produces  lordosis  and 
"  pot-belly."  Further,  the  weakness  of  the  glutei,  as  already  ex- 
plained, causes  a  waddling  gait,  the  legs  being  planted  wide 
apart ;  and  as  we  have  already  seen,  the  mode  of  rising  from 
the  ground  in  such  cases  is  pathognomonic.  Such  a  patient 
when  placed  on  the  ground  and  told  to  get  up  rolls  round  on  his 
face,  then  gets   on   his   hands  and   knees.     Then  to  get  on   his 


Fig.  144.— Muscular  dys- 
trophy in  a  lad  of  17- 
Showing  lordosis. 


POSTURES    AND    GAITS 


301 


feet,  he  extends  the  knees,  and  suddenly,  pressing  his  hands 
on  one  knee  after  the  other,  proceeds  to  extend  the  hips  and 
straighten  the  spine  by  "  dimbing  up "  his  own  thighs  until 
he  reaches  the  erect  posture. 

In  some  cases  of  peripheral  neuritis  without  muscular  paralysis 


Fig.  145.- 


-Case  of  peripheral  neuritis  from 
sesthesia  of  soles. 


'trench-feet,"  with  hyper- 


but  with  acute  hyperaesthesia  of  the  soles,  the  patient  cannot 
bear  to  support  his  weight  on  the  feet.  Standing  and  walking 
are  therefore,  for  a  time,  impossible.  When  recovery  sets  in,  the 
patient  passes  through  a  stage  during  which  he  stands  and  walks 
on  the  heels  only,  keeping  the  front  part  of  the  feet  carefully  off 
the  ground  (see  Fig.  145). 


302 


NERVOUS    DISEASES 


The  posture  and  gait  of  "paralysis  agitans  are  diagnostic,  so 
much  so,  that  patients  have  a  strong  family  resemblance  (see 
Figs.  146  and  147).  In  a  well-marked  case  the  patient  stands 
with  the  trunk  stooping  forwards,  the  face  appearing  "  starched  " 
and  expressionless — the  so-called  "  Parkinsonian  mask,"  in  which 
there  is  little  or  no  emotional  play  of  features.  The 
upper  limbs  are  slightly  abducted  at  the  shoulders,  semi- 
flexed at  the  elbows,  shghtly  extended  at  the  wrists,  flexed 
at  the  metacarpo -phalangeal  joints,  and  extended  at  the 
inter-phalangeal  joints,  as  if  holding  a  pen  —  the  "  in- 
terosseal  "  attitude — and  very  often  they  show 
the  famihar  rhythmic,  "  pill-rolling "  tremor. 
The  tremor  may  affect  the  proximal  joints 
as  well,  and  even  the  lower  limbs,  face, 
jaw,  palate  and  tongue.  All  the  voluntary 
movements  of  the  trunk  and  limbs  are  slow 
and  stif¥,  the  upper  limbs  no  longer  "swing" 
as  the  patient  walks  (in  unilateral  cases  this 
loss  of  swing  is  confined  to  the  arm  of  the 
affected  side),  and  the  gait  is  "  festinant." 
The  patient  moves  forward  with  short,  shufHing 
steps,  and  when  he  turns,  his  trunk  moves 
slowly  en  masse,  as  if  made  of  glass,  whilst 
his  steps  in  walking  tend  to  get  faster  and 
faster,  as  if  he  were  "  chasing  his  own  centre  of 
gravity."  This  is  called  "  propulsion."  Still 
more  frequently  do  we  observe  "  retropulsion," 
in  which  the  patient,  when  pulled  gently  from  behind,  tends  to  run 
backwards  with  short,  hasty  steps.  This  retropulsion  may  sometimes 
be  induced  even  by  the  act  of  looking  upwards.  A  shghter  degree 
of  this  same  posture  and  gait  is  not  uncommon  in  simple  old  age, 
and  may  also  occur  in  pseudo-bulbar  paralysis  and  in  the  multiple 
lacunar  softenings  of  the  brain  described  by  Marie  and  Ferrand. 

The  gait  in  chorea  is  sometimes  peculiar,  partly  owing  to  a 
degree  of  ataxia,  partly  from  the  presence  of  additional  irregular 
involuntary  movements.  Sometimes  one  foot  seems  as  if  it  were 
momentarily  entangled  by  an  invisible  obstacle,  which  holds  the 
child  back  for  an  instant,  the  patient  then  hastily  resumes  his 
forward  progress ;  or  his  knee  may  give  way  suddenly,  causing 
him  to  fall. 


Fig.  146.— Paralysis 

aaritans — bilateral. 


POSTUKES    AND    GAITS 


303 


Many  chronic  epileptics  have  a  peculiar  slouching  posture  and 
gait,  the  posture  of  the  hands,  as  Sprathng  '  has  pointed  out, 
being  specially  characteristic.  The  fingers  are  habitually  flexed, 
and  the  wrists  bent  to  a  right  angle,  and  the  patient  often 
has  a  marked  forward  stoop  of  the  shoulders. 


Fig.  147. — Paralysis  agitans — bilateral. 


Various  deformities  produce  abnormalities  of  gait  and  posture. 
If,  for  example,  one  lower  limb  is  shortened  from  disease  of  the 
bones  or  joints,  from  malformations  such  as  coxa  vara,  or  con- 
genital dislocation  of  hip,  or  from  infantile  paralysis,  the  gait 
becomes  correspondingly  altered. 

1  New  York  Medical  Journal,  1905,  p.  849. 


CHAPTER    XVIII 

TROPHO-NEUROSES 

The  central  nervous  system  exercises  a  profound  influence  on  the 
nutrition  of  all  the  tissues.  There  is,  however,  no  evidence  of 
the  existence  of  special  nerves  whose  function  is  trophic  and 
trophic  only.  The  control  over  nutrition  which  the  nervous  system 
possesses  is  probably  exercised  in  a  complex  fashion,  in  which 
there  are  several  factors  involved.  Striated  muscles,  for  example, 
undergo  atrophy  when  the  cells  of  the  corresponding  motor  nucleus 
in  the  cord  or  medulla  are  destroyed,  or  when  the  motor  nerve- 
fibre  leading  from  the  nerve-cell  to  the  muscle-fibre  is  interrupted. 
The  result  is  muscular  atrophy,  the  different  varieties  of  which  we 
have  already  studied  (see  p.  232).  Afferent  nerve-fibres  conveying 
sensory  impressions,  whether  conscious  or  subconscious^  have  also 
a  profound  influence  upon  tissue-nutrition,  especially  upon  that 
of  the  skin  and  its  appendages.  Therefore  in  anaesthetic  areas 
trivial  injuries  are  liable  to  produce  destructive  tissue-changes. 
Lastly,  the  central  nervous  system  indirectly  influences  the  tissues 
through  their  blood-supply,  by  means  of  its  connections  with  the 
vasomotor  system.  The  vegetative  system  may  also  be  dis- 
ordered primarily,  apart  from  the  central  nervous  system,  not  only 
in  gross  lesions  of  the  sympathetic  chain,  but  also  in  the  so- 
called  angio-neuroses. 

Excluding,  then,  the  muscular  atrophies  and  the  angio-neuroses, 
which  are  studied  elsewhere,  let  us  direct  our  attention  to  certain 
trophic  disorders  which  are  associated  more  or  less  directly  with 
affections  of  the  cerebro-spinal  nervous  system.  Trophic  disorders 
may  be  distributed  widely  all  over  the  body,  or  they  may  be 
limited  to  certain  circumscribed  areas  corresponding  to  a  peri- 
pheral nerve,  to  a  posterior  root,  or  to  some  division  of  the  spinal 
cord  or  brain. 

Generalised  Trophic  Disorders. — Of  these,  one  of  the  best 
examples  is  the  well-known  anorexia  nervosa.  In  this  affection, 
without  evidence  of  structural  disease  of  any  organ,  the  patient 

304 


TROPHONEUROSES  305 

(generally  a  young  woman)  loses  appetite  and  becomes  pro- 
gressively emaciated,  often  to  a  profound  degree.  The  condition 
sometimes  follows  a  shock,  physical  or  mental,  perhaps  an  affaire 
du  cceur,  though  in  other  instances  we  can  find  no  apparent 
exciting  cause.  In  diagnosing  this  condition,  we  have  first  to 
exclude  other  conditions,  such  as  diabetes,  tuberculosis,  and 
malignant  disease,  which  commonly  produce  emaciation.  The 
patient  generally  exhibits  certain  "  stigmata  "  of  functional  disease. 
Of  these  stigmata  the  most  frequent  is  a  hemi-ansesthesia,  usually 
slight  in  degree  and  generally  left-sided  (see  later,  p.  392). 


Fig.  148. — Adiposis  dolorosa  in  a  woman  of  37. 

In  marked  contrast  to  this  is  the  rare  afiection  known  as 
adiposis  dolorosa,  or  Dercum's  disease.  It  occurs  chiefly  in  middle- 
aged  women,  many  of  the  patients  being  alcoholic  or  syphilitic. 
The  patient  is  diffusely  obese,  and,  in  addition,  she  has  localised 
fatty  lumps  in  the  subcutaneous  tissue,  forming  large  pendulous 
swellings,  chiefly  on  the  limbs  and  trunk.  These  swellings  may 
be  symmetrical  or  asymmetrical.  They  appear  and  steadily 
increase  in  size,  and  consist  of  fat  and  of  an  embryonic  form  of 
connective  tissue.      The    arms  are   most   frequently  the  sites   of 

u 


306  NERVOUS   DISEASES 

the  swellings,  which  are  usually  tender  on  pressure  and  may 
have  spontaneous  pains.  Certain  areas,  however,  such  as  the 
hands,  feet,  and  face,  are  always  spared.  The  nerve-trunks  are 
tender,  and  there  may  be  areas  of  blunting  or  loss  of  cutaneous 
sensibility.  Sometimes  the  pituitary  and  thjn-oid  glands  are 
indurated,  but  the  patient  has  none  of  the  mental  or  physical 
features  of  myxoedema,  though  she  often  complains  of  mental 
lassitude  and  asthenia. 

A  curious  condition  of  the  bones  results  from  hypertrophy  or 
functional  over-activity  of  the  anterior  lobe  of  the  pituitary  gland. ^ 
Hyper-secretion  by  this  gland  appears  to  set  free  in  the  body  certain 
abnormal  substances  whose  action"  is  to  cause  an  extraordinary 
growth  of  bony  tissues.  If  the  disease  sets  in  before  the  age  at 
which  the  epiphyses  have  become  joined,  the  bones  grow  enormously 
in  all  their  dimensions,  and  the  result  is  gigantism.  But  if  the 
affection  begins  after  the  epiphyses  have  united,  the  overgrowth 
of  the  bones  is  confined  to  their  ends,  producing  acromegaly. 

The  phenomena  of  acromegaly  are  very  characteristic  (see 
Figs.  149  and  149a).  There  is  a  progressive  enlargement  of  the 
bones  and  soft  parts,  most  marked  in  the  hands  and  feet,  but 
also  affecting  other  parts,  notably  the  skull  and  face.  The  skull 
becomes  enlarged  and  thickened,  all  its  bony  ridges  are  ex- 
aggerated ;  the  margins  of  the  orbits,  the  cheek-bones,  and  most 
striking  of  all,  the  lower  jaw,  become  enlarged.  The  mandible 
becomes  prognathous,  the  lower  teeth  biting  in  front  of  the 
upper,  instead  of  vice  versa,  and  the  teeth  become  widely  separ- 
ated. The  soft  parts  also  share  in  the  hypertrophy.  The  lower 
lip,  nose,  tongue,  uvula,  tonsils,  and  the  cartilages  of  the  ears,  all 
become  enlarged,  and  the  skin  of  the  face  becomes  thick  and  coarse. 
The  hands  and  feet  increase  in  size  (not  the  nails),  so  that  the 
patient  requires  gloves  and  shoes  several  sizes  larger  than  before. 
Spinal  curvature  is  also  present,  usually  a  cervical  kyphosis,  and 
the  thorax,  pelvis,  and  even  the  external  genitals  become  enlarged. 
In  addition,  we  meet  with  symptoms  referable  to  disorder  of  the 
posterior  lobe.     Thus  in  the  early  stage  of  super-pituitarism  there 

1  Acromegaly  cannot  be  ascribed,  as  was  formerly  thought,  to  deficient 
pituitary  secretion,  for  as  Tamburini  and  Modena  have  pointed  out  {Rivista 
sperimentale  di  Freniatria,  1903,  fasc.  3  and  4),  experimental  destruction  of 
the  gland  does  not  cause  acromegaly,  nor  do  malignant  growths  nor  tuber- 
culous disease  of  the  gland  produce  it,  but  only  conditions  such  as  hyper- 
trophy or  adenomatous  hyperplasia. 


TROPHONEUROSES 


307 


is  often  a  spontaneous  glycosuria,  whereas  in  the  later  stage,  when 
symptoms  of  sub-pituitarism  supervene  {e.g.  low  blood-pressure, 
dry  skin,  subnormal  temperature),  there  is  found  a  high  sugar- 
tolerance  (see  p.  32),  so  that  excessive  amounts  of  glucose,  400 
grammes  or  more,  can  be  taken  without  inducing  an  overflow 
glycosuria.     In  female  patients  amenonlifea  occurs. 


Fig.  149. 


Acromegaly  of  eight  years'  duration  in  a  man  aged  42.     The  patient 
had  bi-temporal  hemianopia. 


In  addition  to  these  phenomena  the  patient  complains  of 
severe  headaches,  owing  to  the  intra-cranial  pituitary  tumour. 
This  tumour,  from  its  position  in  the  sella  turcica,  frequently 
encroaches  on  the  adjacent  optic  chiasma,  and  then  there  is 
produced  a  corresponding  alTection  of  the  visual  fields  (see 
p.     132)    usually    commencing    as    a    bi-temporal    hemianopia, 


308 


NERVOUS  DISEASES 


which    may,    as    the     disease    advances,    progress     to    complete 
blindness. 

Apart,  however,  from  pituitary  disease,  which  strictly  speak- 
ing, although  intra-cranial,  is  not  primarily  a  nervous  disorder, 
we  sometimes  have  widespread  overgrowth  of  the  tissues,  confined 
to  one-half  of  the  body  and  probably  of  cerebral  origin.     Fig.  150 


Fig.  150. — Left-sided  hemi-hypertrophy. 

represents  such  a  patient  with  left-sided  hemi-hypertrofhy,  in  whom 
all  the  bones  of  the  left  side  (as  verified  by  skiagrams),  including 
those  of  the  face,  limbs,  pelvis  and  thorax,  together  with  the  soft 
tissues  of  the  face,  tonsil,  tongue  and  testicle,  were  larger  than 
on  the  right  side.  But  the  right  side  of  the  cranium,  and  pro- 
bably also  the  right  side  of  the  brain,  were  larger  than  the  left. 

Passing  next  to  trophic  disorders  of  more  Umited  distribution, 
it  is  convenient  to  discuss  them  in  certain  groups. 


TROPHO-NEUROSES  309 

Trophic  Changes  in  the  Skin  and  its  Appendages  .^6'k»s.s?/ 

skin  is  a  condition  met  witii  chiefly  in  the  hands,  in  certain  cases 
of  long-standing  peripheral  nerve  palsies,  whether  traumatic  or 
neuritic  in  origin.  It  is  also  a  frequent  accompaniment  of  osteo- 
arthritis, not  only  in  the  ordinary  "  rheumatoid  "  variety,  but  also 
in  the  arthritis  which  comes  on  in  hemiplegic  limbs.  The  skin 
of  the  fingers  becomes  thinned  and  atrophic,  with  a  peculiar  smooth, 
shiny  surface.  The  nails  in  many  cases  are  altered,  being  longi- 
tudinally striated  and  excessively  curved  from  side  to  side.  The 
finger-pads  are  wasted  and  the  finger-tips  taper  to  a  point,  as  is 


Fig.  151. — -Right-sided  brachial  neuritis  with  glossy  skin  and  tapering  finger-tips. 

seen  in  Fig.  151,  which  is  taken  from  a  case  of  right-sided  brachial 
neuritis. 

Perforating  ulcers  occur  most  typically  in  tabes  dorsahs.  They 
are  generally  situated  on  the  foot,  on  its  plantar  surface,  especially 
at  the  metatarso -phalangeal  joint  of  the  great  or  httle  toe.  They 
may  also  occur  under  the  heel  or  under  the  terminal  phalanx  of 
the  hallux.  Each  ulcer  begins  as  a  thickening  of  the  epidermis, 
like  a  corn.  Suppuration  occurs  under  this,  and  the  pus  finds 
its  way  out  through  a  small  opening  in  the  centre  (Fig.  152). 
A  narrow  sinus  is  thus  formed  which  increases  in  depth  until  it 
may  extend  into  the  joint  beneath,  which  is  often  disorganised, 
and  carious  bone  may  be  felt  at  the  bottom.     Sometimes  the  ulcer 


310 


NERVOUS    DISEASES 


heals  up  under  treatment.  The  tabetic  perforating  ulcer  is  pain- 
less. Somewhat  similar  trophic  ulcers  are  met  with  in  certain 
cases  of  spina  bifida  occulta  and  also  in  syringomyelia,  but  in  this 
latter  disease  they  are  commoner  in  the  hands.  Diabetic  neuritis 
is  also  occasionally  associated  with  perforating  ulcers  of  the  feet, 
a  minor  variety  of  diabetic  gangrene.  In  lejprous  neuritis  per- 
forating  ulcers    are  not  infrequent,   though  it    is    commoner  to 


Fig.  152. — Perforating  ulcers  in  tabes. 

have  a  still  more  extensive  loss  of  tissue,  whole  phalanges 
disappearing  from  the  fingers  and  toes.  Painless  whitlows — in  so- 
called  "Morvan's  disease,'"  a  sub-variety  of  syringomyeha,  are 
found  at  the  finger-tips.  These  whitlows  are  sometimes  the  result 
of  trivial  injuries  which  in  a  normal  individual  would  not  produce 
any  serious  results.  In  other  cases  the  explanation  is  found  in 
the  absence  of  sensibility  to  temperature  and  pain,  which  is 
characteristic  of  the  disease,  so  that  the  patient  burns  the  fingers 
painlessly  and  produces  bhsters  and  even  areas  of  sloughing. 


TROPHO-NEUROSES  31 J 

In  certain  cases  of  tabes  there  may  be  a  perforating  ulcer  in 
the  mouth.  First  the  teeth  become  loosened  and  fall  out,  then 
the  alveolar  margin  of  the  jaw  is  absorbed,  and  if  the  upper  jaw 
be  affected  a  perforation  into  the  nasal  cavity  may  be  established. 

Herpes  zoster  is  a  very  typical  example  of  a  trophic  cutaneous 
disorder  which  has  a  direct  nervous  origin,  viz.,  inflammation  or 
thrombosis  of  the  corresponding  posterior  root  ganglion.  In  this 
affection  a  crop  of  vesicles  appear,  which  are  distributed  in  a 
definite  metameric  area,  corresponding  to  the  posterior  root 
whose  ganglion  is  diseased.  In  the  case  of  facial  herpes  it  is  the 
Gasserian  ganglion  which  is  inflamed,  in  whole  or  in  part,  whilst 
herpes  of  the  external  auditory  canal  is  associated  with  in- 
flammation of  the  geniculate  ganglion.  The  herpetic  vesicles 
usually  become  pustular  and  subsequently  permanent  scars  may 
remain.  Herpes  is  sometimes  preceded,  for  a  day  or  two,  by  pre- 
herpetic  pain  in  the  area  in  which  the  eruption  is  about  to  appear  ; 
and  not  infrequently  the  eruption  is  followed  by  prolonged  and 
intractable  post-herpetic  neuralgia.  Figs.  153  and  153a  are  from  a 
typical  case  of  herpes  in  the  area  of  the  fifth  thoracic  root. 
Sometimes  herpes  develops  in  the  course  of  diseases  of  the 
vertebrae  or  of  the  spinal  meninges.  Such  an  occurrence  signifies 
that  the  morbid  process  has  attacked  the  corresponding  posterior 
root  ganghon  or  gangHa.  Even  in  simple  herpes  zoster  we  can 
sometimes  elicit  Kernig's  sign^  (see  p.  68). 

Bed-sores  result  from  inflammatory  and  destructive  changes  in 
the  skin  and  underlying  tissues  of  bedridden  patients,  whether  in 
persons  merely  enfeebled  by  prolonged  illness  (especially  in  enteric 
fever)  or,  more  commonly,  in  severe  organic  paralysis,  such  as 
hemiplegia  or  paraplegia.  Most  bed-sores,  occurring  as  they  do 
at  the  sites  of  pressure,  can  be  prevented  by  careful  nursing,  by 
keeping  the  patient's  skin  scrupulously  clean  and  dry,  by  placing 
him  on  a  water-bed,  and  by  hardening  the  epidermis  by  local 
applications  of  methylated  spirit.  But  sometimes  in  spite  of  the 
most  assiduous  nursing,  bed-sores  may  develop  within  a  few  days 
or  even  within  a  few  hours  of  an  initial  paraplegia  or  hemiplegia. 
This  so-called  acute  decubitus  is  of  grave  omen. 

^  This  fact,  together  with  the  frequent  occurrence  of  lymphocytosis  of  the 
cerabro-spinal  fluid,  shows  that  in  herpes  zoster  the  pathological  process  is  not 
necessarily  limited  to  the  posterior  root-ganglion,  but  is  part  of  a  more  widely 
diffused  meningeal  irritation. 

Bilbeza,  Archives  generales  de  Med.,  Feb.  27,  1906. 


312 


NEKVOUS   DISEASES 


The  commonest  site  for  a  bed-sore  in  a  hemiplegic  patient  is 
over  the  great  trochanter  on  the  paralysed  side.  In  paraplegia 
from  cord  lesions,  e.g.  acute  myelitis,  the  bed-sore  commonly  forms 
over  the  middle  of  the  sacrum  (Fig.  154).  A  bed-sore  commences 
as  an  area  of  redness  of  the  skin,  bullae  then  develop  and  burst, 
leaving  an  ulcerating  or  sloughing  surface  beneath.     The  sloughing 


FIG.1153. 

Herpes  zoster  in  area  of  fifth 
dorsal  root.  Second  day  after 
appearance  of  eruption. 


Fig.  153A. 

Herpes  zoster — the  same  patient  as  in 
Fig.  153.  Eruption  surrounds  the 
nipple,  and  thence  extends  inwards 
to  mid-sternum. 


process  may  extend  down  to  the  periosteum  and  bones,  and  in 
sacral  decubitus  the  infection  may  extend  into  the  vertebral 
canal,  producing  a  fatal  cerebro-spinal  meningitis,  septic  organisms 
gaining  access  not  only  from  the  skin,  but  from  the  intestinal  dis- 
charges. Bed-sores  are  also  met  with  in  advanced  cases  of 
bedridden  dementia,  even  where  there  is  no  paralysis.  In  these 
patients,  as  in  cases  of  prolonged  fever,  the  sores  develop  on 
the  pressure  points,  viz.  the  heels,  hips,  backs  of  the  scapulae 
and  even  on  the  inner  sides  of  the  knees.      We  also   meet  with 


TROPHO-NEUROSES 


313 


excoriations  of  the  skin,  which  may  amount  to  bed-sores,  in 
cases  of  violent  chorea  in  which  the  patient  knocks  his  Hmbs 
against  surrounding  objects. 

Before  leaving  the  subject  of  destructive  trophic  lesions  of  the 


1^1 


Fig.  154. — Luiubo-sacral  myelitis  with  sacral  bed-sore  or  decubitus. 
Showing  atrophy  and  paralysis  of  muscles  below  left  knee.  The 
small  chart  on  the  right  indicates  the  coexisting  area  of  anEesthesia. 

skin,  we  must  mention  symmetrical  gangrene,  a  localised  gangrene 
chiefly  occurring  in  the  tips  of  the  fingers  and  toes,  and  preceded 
by  pains  or  parsesthesias  of  the  parts.  But  to  this,  the  most  severe 
phase  of  Raynaud's  disease,  we  shall  refer  again  when  we  con- 
sider the  angio-neuroses. 

The  commonest   points    of   incidence    of   rodent  ulcers  on  the 


314  NERVOUS   DISEASES 

face  are,  as  Cheatle  "^  has  shown,  at  the  positions  where  the 
various  branches  of  the  trigeminal  nerve  become  cutaneous, 
especially  over  the  points  of  emergence  of  the  infra-orbital,  infra- 
trochlear,  temporo-malar  and  lachrymal  nerves,  and  also  with 
particular  frequency  at  the  inner  canthus  of  the  eye  and  at  the 
angle  where  the  ala  nasi  joins  the  cheek.  He  has  also  shown 
that  these  spots  are  the  favourite  points  of  incidence  of  leuco- 
derma  and  scleroderma.  The  precise  significance  of  these  facts 
is  still  obscure,  but  Cheatle  has  also  recorded  the  curious  fact 
that  rodent  ulcers  are  frequently  limited  to  the  distribution  of 
normal  nerve-areas  and  that  the  spread  of  a  rodent  ulcer  ceases 
abruptly  when  it  reaches  a  cutaneous  area  which  has  become 
denervated  by  division  of  its  sensory  nerves. 

There  are  other  trophic  lesions  unaccompanied  by  necrosis  or 
ulceration,  and  consisting  in  local  changes  affecting  one  or  more  ele- 
ments of  the  skin  or  subcutaneous  tissues,  whether  in  the  direction 
of  atrophy  or  of  hypertrophy.  Perhaps  the  most  typical  examples 
of  this  variety  are  scleroderma,  leucoderma,  and  cutaneous  nsevi. 
Scleroderma  is  a  disease  in  which  the  skin  becomes  abnormally  hard 
and  fibrous.  The  condition  may  be  diffuse  or  circumscribed.  In 
the  rarer  diffuse  variety,  large  areas  of  skin,  usually  symmetrical; 
and  especially  on  the  upper  limbs,  become  hard  and  rigid,  losing 
their  elasticity  so  that  the  affected  sldn  can  no  longer  be  pinched 
up  with  the  fingers.  Sometimes  there  is  a  prehminary  oedematous 
stage.  As  the  disease  advances,  the  sclerotic  process  may  extend 
to  deeper  structures  such  as  tendons,  and  this,  with  the  rigidity  of 
the  skin,  limits  the  movements  of  the  joints  and  may  produce 
permanent  deformities.  If  the  fingers  are  affected,  they  become 
tapering  at  the  tips  and  permanently  flexed.  If  the  face  is  affected, 
it  becomes  immobile  and  mask-like.  Circumscribed  scleroderma,  or 
morphoea,  is  the  commoner  variety,  in  which  small  patches  of  skin 
become  hard,  white  and  ivory-hke,  the  distribution  of  the  patches 
being  somewhat  similar  to  those  of  herpes  zoster — i.e.  meta- 
merically,  in  the  area  of  a  posterior  root,  or  of  one  of  the  divisions 
of  the  trigeminal  nerve  on  the  face. 

Leucoderma,  or  disappearance  of  pigment  from  circumscribed 
patches  of  skin,  is  also  commonly  distributed,  more  or  less, 
in  nerve-areas.  The  patch  of  absolute  paUor  has  a  pigmented 
edge    where   it   joins   the   normal  skin,  and  it   tends   to   spread 

1  Brit.  Med.  Journal,  April  29,  1905, 


TR0PH0-NEUR08ES 


315 


slowly  along  the  particular  area.  This  disease  is,  of  course,  most 
striking  when  it  affects  patients  of  sallow  complexion  or  of  dark- 
skinned  race.  Leucoderma  also  occurs  in  the  maculo-anaesthetic 
type  of  leprosy,  where  the  leucodermic  patches  are  often  red  and 
hypersesthetic  at  the  edges  and  anaesthetic  in  the  centre. 

Figs.   155  and  155a  represent  a  little  girl  aged  eight,  in  whom 


Fig.  155.  Fig.  155a. 

Congenital  verrucosis  of  metameric  distribution. 


patches  of  warty  growths  were  distributed  metamerically  on  the 
limbs  and  trunk. 

Congenital  cutaneous  nwvi — "  port-wine  stains  " — are  also  com- 
monly distributed  in  root  areas  on  the  trunk  or  in  the  trigeminal 
distribution  on  the  face.  The  trigeminal  area  is  afiected  with 
special  frequency,  one,  two,  or  all  three  divisions  of  the  trigeminal 
being  mapped  out,  more  or  less  accurately.  It  is  an  interesting 
fact    that   a   cutaneous    nsevus    on   the    face    may   be  associated 


316 


NERVOUS    DISEASES 


with  hypertrophy  of  the  subjacent  deep  tissues,  with  enlargement 
of  the  eyeball,  and  even  with  a  nsevoid  condition  of  the 
nasal  mucous  membrane  and  of  the  dura  mater  on  the  correspond- 
ing side,  all  of  which  structures  are  innervated  by  the  trigeminal 
nerve.  More  than  this,  cases  of  naevus  of  the  face  may  be  asso- 
ciated with  recurrent  epistaxis  from  the  nsevoid  nasal  mucosa,  and 


Fig.  156.  Fig.  156a. 

von  Recklinghausen's  disease  in  a  man  aged  38. 

sometimes  they  develop  sudden  infantile  hemiplegia  with  epilepti- 
form convulsions,  due  to  sub-dural  hsemorrhage  from  the  dural 
nsevus.-^ 

Large  neuro -fibromata — ^so-called  plexifoi^m  neuroma  or  ele- 
phantiasis nervorum — are  more  common  on  the  trigeminal  nerve, 
especially  in  its  upper  divisions,  than  on  any  other  nerve  of  the 
body.  Such  a  tumour  is  generally  part  of  a  more  widespread 
affection  known  as  von  Recklinglumsen'' s  disease  (see  Figs.  156,  156a). 

^  Gushing,  Journal  of  American  Med.  Association,  1906,  p.  178. 


TROPHO-NEUROSES  317 

In  this  disease  we  find,  in  a  complete  case,  neuro-fibromata,  often 
of  fairly  large  size,  forming  painless  swellings  on  the  face  or  else- 
where, together  with  multiple  soft  fibromata  of  the  skin  forming 
sessile  or  pedunculated  growths  (known  as  molluscum  fibrosum) 
and  also  patches  of  cutaneous  pigmentation  distributed  more  or 
less  definitely  in  nerve  areas.     The  neuro-fibromata  of  von  Reck- 


FlG.  157.— Case  of  left-sided  hemiplegia  with  hemorrhages  under  all 
the  finger-nails  on  the  left  side,  and  under  the  nail  of  the  right 
little  finger. 

linghausen's  disease  do  not  cause  symptoms  except  by  accidental 
mechanical  compression  of  adjacent  structures.  The  disease,  which 
sometimes  runs  in  famiUes,  often  appears  in  childhood  and  remains 
stationary  for  many  years,  when  it  may  suddenly  resume  its  spread, 
new  tumours  cropping  out  all  over  the  body. 

Various  cutaneous  lesions  are  present  in  many  cases  of  arsenical 
neuritis.  A  brownish  macular  pigmentation  of  the  skin  is,  of 
course,  common  in  chronic  arsenical  poisoning,  without  neuritis. 
But  in  arsenical  neuritis  we  frequently  observe  special  cutaneous 


318  NERVOUS    DISEASES 

affections,  such  as  glossy  skin,  herpes  zoster,  falling  of  the  hair, 
and  most  characteristic  of  all,  hyperkeratosis  of  the  palms  and 
soles,  where  the  epidermis  becomes  much  thickened  and  tends  to 
desquamate.  In  addition  to  these  skin  lesions,  we  have  the 
ordinary  signs  of  a  peripheral  neuritis,  such  as  drop-wrist,  drop- 
foot,  &c. 

There  is  a  rare  trophic  affection  of  the  skin,  described  by 
Gowers  as  local  'panatrophy,  in  which  certain  circumscribed  areas 
of  the  face,  trunk,  or  hmbs,  varying  in  size  from  the  diameter 
of  a  cherry  to  that  of  an  orange,  undergo  local  atrophy  of  all  the 
subcutaneous  tissues  down  to  the  bone,  the  skin  becoming  also 
slightly  thinned.  These  patches  look  like  subcutaneous  excava- 
tions, and  although  trophic  in  origin,  they  do  not  correspond  to 
regular  nerve-areas  but  are  quite  irregularly  distributed. 

Progressive  descending  lipo-dystrophy  ^  is  another  rare  trophic 
disorder,  confined  to  the  female  sex  and  commencing  at  ages 
varying  from  ten  to  thirty  years.  In  this  malady  the  subcutaneous 
fat  disappears  from  the  face  and  neck,  and  later  from  the  upper 
limbs  and  trunk.  In  the  case  shown  in  Eig.  158  the  process  of  fat- 
absorption  advanced  from  above  downwards  at  the  rate  of  about 
one  inch  every  year.  The  lower  limbs  and  buttocks,  on  the  other 
hand,  remain  plump,  and  may  even  be  excessively  fat.  The  eyes 
become  sunken  from  disappearance  of  orbital  fat,  although  this 
is  not  constant.     The  mammary  fat  may  remain  unaffected. 

Trophic  changes  are  sometimes  present  in  the  hair.  Hyper- 
tricliosis,  or  excessive  growth  of  the  hair,  is  met  with  most  fre- 
quently on  "  hairy  moles,"  which  are,  moreover,  excessively 
pigmented  in  the  skin  as  well.  It  is  important  to  remember  that 
a  hairy  mole  in  the  lumbo-sacral  region  is  often  an  indication  of  a 
spina  bifida  occulta.  Local  hypertrichosis  also  occurs  occasionally 
in  other  nerve-areas.  The  hair  may  also  be  affected  in  various  ways 
in  other  nervous  affections.  Well- authenticated  cases  have  been 
recorded  of  blanching  of  the  hair  of  the  scalp  within  a  few  hours, 
as  a  result  of  profound  emotion.  It  is  not  uncommon  to  meet 
with  patches  of  whitened  hair  in  nerve-areas  which  have  been 
the  site  of  severe  neuralgia.  Even  in  the  ordinary  greyness  of 
advancing  years,  and  in  the  idiopathic  premature  greyness  of 
youth,    as   Cheatle  ^   pointed   out,    the   maximum   greyness   often 

1  Parkes  Weber,  Brit.  Med.  Journal,  1913,  p.  1154. 

2  Brit.  Med.  Journal,  July  22,  1905. 


PLATE   II. 

Sub-ungual  hteuiorrhagus  iu  a  woman  aged  42  in  whom,  eighteen 
months  after  an  attack  of  left  hemiplegia,  there  occurred  acute  swelling 
and  redness  of  the  left  hand,  to  a  lesser  degree  in  the  left  foot,  and, 
a  few  days  later,  in  the  right  little  finger.  The  finger-tips  became 
deeply  cyanosed,  bullas  developed  on  the  hand,  and  were  followed  by 
desquamation. 

-  The  drawing  shows  the  condition  two  and  a  half  months  later,  the 
nails  having  grown  to  some  extent.  The  left  hand  was  hotter  than  the 
tight,  and  perspired  more  freely. 


To  face  page  318. 


)'t9W  bajs  ibam 


TROPHO-NEUROSES 


319 


appears  in  nerve-areas  in  the  scalp  and  beard.  There  is  a  variety 
of  localised  alopecia  in  which  the  hair  falls  out  suddenly  in  a  certain 
nerve  area.     Many  patients  with  exophthalmic  goitre,  as  Wal.sh 


Fig.  158. — Descending  lipo-dystrophy. 

pointed  out,^  have  a  band  of  alopecia  at  the  frontal  end  of  the  scalp. 
Hypertrichosis  of  the  eyebrows  is  sometimes  associated  with 
hyperthyroidism,  whilst  a  varying  degree  of  supra-ciliary  alopecia  is 

1  Lancet,  1907,  p.  1080. 


320 


NERVOUS   DISEASES 


one  of  the  signs  of  thyroid  insufficiency  (signe  de  sourcil),^  and  affords 
an  indication  for  thyroid  medication.  We  occasionally  meet  with 
cases  of  universal  alopecia,  in  which  the  hairs  all  over  the  body 
fall  out,  and  the  patient  may  remain  permanently  hairless,  his 
skin  meanwhile  being  considerably  thinned. 

Trophic  changes  in  the  nails  occur  in  a  number  of  nervous 
diseases.      Sometimes    the    nails    become    hypertrophied,    as 


m 


FIO.  159.  FIG.  159  A. 

Right-sided  facial  hemiatrophy,  also  implicating  the  coiTesponding  side 
of  the  tongue. 

the  toe-nails  of  patients  with  chronic  paraplegia  from  any  cause. 
In  peripheral  neuritis,  especially  the  arsenical  variety,  we  may 
meet  with  excessive  curving,  brittleness,  atrophy  and  even  falhng 
of  the  nails.  In  tabes  the  toe-nails,  especially  those  of  the  big  toes, 
are  sometimes  shed,  whilst  in  some  cases  of  cerebral  hcemorrhage  we 
find  haemorrhages  under  the  nails  of  the  hemiplegic  hand  (Fig. 
157  and  Plate  II.).  As  the  nail  grows,  the  hsemorrhagic  area 
is  gradually  cast  off. 


1  Michel,  These  de  Paris,  1911. 


TROPHONEUROSES 


321 


Trophic  Changes  in  Bones  and  Joints. — An  affection  which 
possesses  characters  common  to  this  group  and  to  the  group  of 
cutaneous  trophic  lesions  is  'progressive  facial  honiatrophy.  It  is 
probably  referable,  as  we  have  already  seen,  to  a  lesion  of 
the  trigeminal  nerve  or  nucleus.  Not  only  is  the  skin  on  the 
affected  side  of  the  face  atrophied  and  wrinkled,  but  the  bones, 
and  especially  the  lower  jaw,  become  smaller  (Figs.  159  and  159a). 


Fig.  160. — Hemi-hypertrophy  of  right  side  of  face. 


Still  more  rarely,  we  meet  with  cases  of  facial  hemi-hypertrophy, 
in  which  the  bones  and  soft  parts  of  one  side  of  the  face  become 
progressively  larger.  In  the  case  shown  in  Fig.  160,  the  enlargement 
of  the  face  followed  an  injm-y  to  the  forehead  in  childhood  on 
the  side  which  afterwards  became  enlarged. 

It  is  not  uncommon  to  find  atrophic  changes  in  the  bones  of 
paralysed  limbs.  In  paralytic  affections  of  children,  whether  of 
the  upper  neurone  type,  as  in  infantile  hemiplegia  (Fig.  161),  or  of 
the  lower  neurone  type,  as  in  acute  anterior  poliomyelitis  (Fig.  162), 
the  bones  of  the  paralysed  limb  become  arrested  in  their  growth 

X 


322 


NERVOUS    DISEASES 


and  are  smaller  in  all  their  dimensions  than  are  the  healthy  limbs. 
Even  in  some  cases  of  hemiplegia  in  adults  the  bones  of  the 
paralysed  limbs  become  excessively  brittle.  I  remember  a  case 
of  hemiplegia  in  a  middle-aged  woman  in  wh<^m  moderate  passive 


Fig.  161. — Old  infantile  hemiplegia, 
left-sided,  with  arrested  growth  of 
limbs. 


Fig.  162. — Old  poliomyelitis  anterior 
acuta.  Paralysis  and  atrophy  of  biceps, 
triceps,  and  deltoid  on  left  side,  with 
ai'rested  growth  of  humerus. 


movements  under  an  anaesthetic,  during  an  attempt  to  break  down 
adhesions  in  the  hip-joint  of  the  hemiplegic  side,  caused  a  fracture 
of  the  neck  of  the  femur.  The  brittleness  of  the  bones  in  certain 
insane  patients  and  their  liability  to  fractures  from  trivial  injuries 
are  well  known.  Moreover,  there  is  a  rare  disease  known  as 
idiopathic  fragilitas  ossium,  in  which  the  patient,  otlierwise  healthy, 
may  fracture  his  bones  from  minimal  accidents,  as,  fqr  examp]©. 


TROPHO-NEUROSES 


323 


where  a  lad  fractured  his  humerus  by  throwing  a  cricket-ball. 
Similar  spontaneous  fractures  also  occur  in  certain  cases  of  labes 
and  of  syringomyelia,  but  in  these  two  diseases  the  fractures  are 
painless,  so  that  the  patient  may  continue  to  use  the  fractured 
limb  in  a  fashion  impossible  to  a  normal  individual. 


Fig.  163. — Tabetiu  arthropathy  of  both  knees  and  of  right  foot.     The  patient's 
right  leg  is  tied  to  the  chair  to  prevent  involuntary  tabetic  movements. 

The  most  typical  trophic  changes  in  joints — the  so-called 
arthropathies,  are  met  with  in  tabes  (constituting  Charcot's  joint), 
in  syringomyelia,  and  in  some  cases  of  leprosy.  In  tabetic  cases 
well-marked  syphilitic  arterial  changes  have  been  found  in  the 
affected  joints.  Hence  it  is  probable  that  vascular  rather  than 
purely  nervous  influences  are  the  primary  cause  of  such  arthro- 
pathies.^   The  large  joints  are  more  liable  to  be  affected,  the  knee 

^  Barre,  J.  G.  Psychologic  unci  Neil,rologie,  1913,  ff.  5  and  0. 


324 


NERVOUS    DISEASES 


and  tlie  tarso-metatarsal  joint  being  the  joints  most  commonly 
attacked    in    tabes    (Fig.    163),    the    shoulder   in   syringomyelia 

(Figs.  164  to  166).  But  in  tabes 
even  the  smaller  joints  may  be 
affected,  as  in  the  patient  shown 
in  Fig.  168,  the  terminal  joint 
of  whose  thumb  was  thus  dis- 
eased. Female  tabetics  seem  to 
be  relatively  more  liable  than 
male  patients  to  osteopathies 
and  arthropathies.  The  exciting 
cause  of  a  tabetic  arthropathy 
i  is  often  some  trivial  traumatism, 

such  as  a  twist   or  sprain  in  a 
joint  in  which  the  sense  of  pain 
is  diminished  or  lost,  hence  the 
\  greater  frequency  of    tabetic  ar- 

>  thropathies  in  the    lower  hmbs. 

■  ^  The  joint  swells  without  pain, 
and  rapid  destructive  changes 
occur  in  its  articular  surfaces, 
which  become  eroded  and  may 
disappear,  together  with  con- 
siderable parts   of    the   adjacent 


Fig.  164. — Syringomyelia  with  arthro- 
pathy of  left  shoulder-joint.  Atrophy 
of  intrinsic  muscles  of  leftj^hand. 

bones.     Fractures  of  the  articular  ends 

are   common,  both  in  tabetic   and  in 

syringomyelic    joints.      The    ligaments 

become  lax  and  the  joint  abnormally 

mobile,   so  that  in   the  knee  we  may 

be    able    to    produce    lateral    passive 

movements,     or    even    to    bend    the 

joint  into  all  sorts  of  curious  positions 

(Fig.    169).     The   joint    is    sometimes 

distended    with    a    glairy     gelatinous 

fluid,  which  may  be  blood-stained.     In  the  later  stages  this  fluid 

may  be  reabsorbed,  throwing  into  relief    the    deformity   of  the 


Fig.  165. — The  same  case  of 
syringomyelia.  Showing 
the  area  of  therm-anaes- 
thesia and  analo-esia. 


TROPHO-NEUROSES 


325 


bones  (Fig.    170).     But  the  changes  in    such    arthropathies   are 
not    entirely     destructive.       Osteophytic    outgrowths    are    often 

formed  in  the  peri-articular 
tissues,  causing  irregular 
thickening  of  the  bones, 
and  producing  little  islands 
of  new  bone  amongst  the 
tissues  around  the  joint. 
These  can  be  readily  de- 
tected on  palpation  and 
verified  by  skiagrams  (Figs. 
171  and  172). 

In  leprosy,  arthropathies 

are  commonest  in  the  fingers 

Fig.  1G6.  —  Syringoruyelia  (same  case  as 
Fig.  1G4).  Kadiogram  of  shoulder- 
joint.  Showing  fracture  of  upper  end 
of  humerus,  also  osteophytic  outgrowth 
from  axillary  border  of  scapula. 

and  toes,  and  perforating  ulcers,  with 
sinuses  leading  into  the  disorganised  joints, 
are  much  commoner  than  in  tabes  or 
syringomyelia.  Hypertrophic  changes  in 
leprous  arthropathies  are  usually  absent, 
the  process  being  purely  destructive. 

Joint  affections  of  a  different  land 
are  met  with  in  some  cases  of  chronic 
hemiplegia.  The  joints  of  the  paralysed 
hmbs  become  swollen  and  deformed  two 
or  three  weeks  after  the  hemiplegic 
attack.  But,  unhke  the  tabetic  and 
syringomyehc  arthropathies,  hemiplegic 
joint-affections  are  acutely  painful. 
Moreover,  the  changes  in  hemiplegic 
joints  are  not  destructive  but  more  of 
the  nature  of  a  subacute  osteo-arthritis, 
with  pain  and  rigidity  on  passive  move- 
ments and  with  a  tendency  to  the 
formation  of  fibrous  adhesions  within 
the    joint    and     to     thickening    of    the 

joint    capsule.     When    the    fingers    are    affected,   they    lose    their 
normal  outline   and   become   clumsy-looking  and   "  sausagy "   in 


Fig.  167.  —  Sj-ringomyelia 
with  arthropathy  of  left 
shoulder-joint,  the  limb 
being  swollen  and  dis- 
placed downwards  en 
masse  at  the  shoulder. 


326 


NERVOUS    DISEASES 


Fig.  liJS. — Tabetic  arthropathy  of  left  thumb. 


Fig.  169. — Tabetic  arthropathy  of  knee-joints. 


TROPHO-NEUROSES 


327 


appearance.  Together  with  this  hemiplegic  arthritis  it  is  not 
uncommon  to  have  a  degree  of  muscular  wasting,  but  without 
electrical  reactions  of  degeneration. 

Finally,  we  must  bear  in  mind  that  certain  hysterical  patients 
complain  of  joint-pains,  usually  mono-articular,  which  may  more 
or  less  closely  simulate  organic  joint  disease.  The  patient  is 
commonly  a  young  woman  who,  after  seme  local  injury  to  the 


Fig.  ltj9A. — Leprosy.  Showing  absence  o£  terminal  phalanges 
of  nearly  all  the  digits.  Kiidimentary  nails  persist  at  the 
ends  of  all.  The  remnant  of  the  terminal  thumb  phalanx 
is  bent  to  an  acute  angle.  Leprous  keratitis  is  present, 
with  ectropion  of  lower  lids.  The  eyebrows  are  absent. 
The  bridge  of  the  nose  is  depressed. 


joint,  or  after  some  emotion,  or  perhaps  from  being  acquainted 
with  another  patient  who  has  joint  disease,  suddenly  complains 
of  intense  joint-pain,  together  with  cutaneous  hypersesthesia  in 
that  region.  The  joint  is  rigid  and  resistant  to  passive  move- 
ment, and  if  the  condition  has  persisted,  as  is  sometimes  the 
case,  for  weeks  or  months,  fibrous  adhesions  may  form.  But 
there  is  no  true  swelling  of  the  joint  when  compared  with  the 
corresponding  hmb  of  the  opposite  side,  although  a  false  appearance 


328 


NERVOUS    DISEASES 


of  swelling  may  appear  to  be  present  owing  to  disuse-atrophy  of 
the  adjacent  muscles.     The  presence  of  other  hysterical  "  stigmata  " 


Fig.  170. — Syringomyelia  with  arthropathy  of  right  shoulder-joint,  and 
destruction  of  head  of  humerus.     Well-marked  scoliosis. 


Fig.  171. — Tabetic  arthropathy  of  elbow-joint.     Radiogram 
showing  bony  deposits  in  the  tissues  around  the  joint. 


often  aids  in  the  diagnosis,  but  an  accurate  opinion  is  sometimes 
a   matter   of   considerable   difficulty  and  is  arrived  at  by  a  pro- 


TROPllO-NEUROSES  320 

cess  of  exclusion.     Accomplished  surgeons  have    been    known  to 
operate  on  such  joints  and  only  on  opening  the  joint  to  discover 


Fig.  172. — Radiogram  of  tabetic  arthropathy  of  knee,  from 
patient  shown  in  Fig.  163.  Showing  disappearance  of  articular 
surfaces  and  presence  of  bony  deposits  in  peri-articular  tissues. 

the  absence  of  organic  disease.  Fortunately,  the  usual  result  of 
such  operations,  if  aseptic,  is  that  the  patient  recovers  from 
her  pains. 


CHAPTER   XIX 

REFLEXES 

For   clinical   purposes    we   have   to    consider   three   varieties    of 
reflexes  : — 

(1)  Superficial  or  skin  reflexes,  e.g.  the  plantar  reflex. 

(2)  Deep,  tendon,  or  osseous  reflexes,  e.g.  the  knee-jerk. 

(3)  Organic    or    visceral    reflexes,    e.g.    vomiting,    micturition, 

parturition. 

Of  these  three  groups,  the  first  two  have  to  do  with  striated 
voluntary  muscles.  They  have  their  reflex  centres  within  the 
cerebro-spinal  axis,  and  many  of  them  can  be  inhibited  by  voluntary 
effort.  The  third  group,  that  of  the  visceral  reflexes,  is  concerned 
not  with  voluntary  muscles  alone,  but  also  with  involuntary  non- 
striated  muscles  which  are  controlled  by  the  vegetative  nervous 
system  and  are  incapable  of  direct  voluntary  restraint — e.g.  the 
muscular  walls  of  the  stomach,  bladder,  rectum,  or  uterus.  Such 
visceral  reflexes  can  be  performed,  more  or  less  perfectly,  inde- 
pendently of  the  central  nervous  system.  Normally,  visceral 
functions  go  on,  for  the  most  part,  unconsciously.  But  even 
they  may  occasionally  evoke  consciousness,  as  when  visceral  pain 
occurs,  or  when  striated  voluntary  muscles  are  required  to 
supplement  an  act  originally  initiated  by  non-striated  muscles, 
or  when  the  reflex  act  causes  stimulation  of  a  cerebro-spinal 
sensory  nerve.  Thus,  to  take  an  example,  the  act  of  defsecation 
is  practically  unconscious  and  uncontrollable,  so  far  as  the  move- 
ment of  the  large  intestine  is  concerned.  But  when  the  lower  end 
of  the  anal  canal  has  its  mucosa  stimulated,  the  perineal  muscles 
come  into  action,  the  act  then  rises  to  consciousness  and  is  more 
or  less  under  control. 

Skin  Reflexes. — These  are  movements  obtained  by  slight  stimu- 
lation of  certain  areas  of  skin  or  mucous  membrane.  The  result 
is  a  movement,  quick  or  slow,  of  the  skin  near  the  point  of  stimula- 
tion, but  not  exactly  under  it.  In  certain  animals  such  as  the 
horse,  skin  reflexes  can  be  obtained  by  touching  almost  any  part 

330 


REFLEXES 


331 


of  the  trunk.  But  in  man  the  skin  as  a  whole  is  less  mobile,  and 
it  is  usually  only  from  certain  special  areas  that  skin  reflexes  can 
be  elicited.  If  the  stimulus  be  too  strong,  it  may  cause  a  reflex 
so  violent  as  to  involve  almost  all  the  voluntary  muscles  of  the 
body.  Or  if  the  stimulus,  even  though  slight,  be  a  painful  one,  as 
for  example  a  pin-prick,  the  result  is  a  rapid  "  defensive  "  move- 
ment— e.g.  sudden  flexion  of  a  limb  or  abrupt  closure  of  the  eye 
(see  "  Defensive  Reflexes,"  p.  229).  The  defensive  reflexes  are 
usually  exaggerated  in  pyramidal  disease. 

The  following  table  gives  a  list  of  the  chief  skin  reflexes  which 
are  of  clinical  importance,  and  the  mode  of  testing  each.  All 
are  more  easily  elicited  in  young  people  than  in  old ;  in  fact, 
if  we  wish  to  demonstrate  the  skin  reflexes  with  certainty,  we 
select  a  child  for  our  subject. 


Method  of  Eliciting. 

Result. 

Segmental 
Level. 

Corneal    .... 

Touching  cornea. 

Orbicularis  oculi  contracts. 

rharyngeal .     .    . 

Touching  posterior  wall  of  pharynx. 

Pharynx  contracts. 

Palatal    .... 

Touching  soft  palate. 

Palate  is  elevated. 

Scapular.     .    .     . 

Stroking  skin  in  inter-scapuhir  region. 

Scapular  muscles  contract. 

C5  to  Thl. 

Epigastric    .     .     . 

Stroking  downwards  from  nipple. 

Epigastrium    dimples    on    side    of 
stimulus. 

Th7  to  Th9. 

Abdominal  .     .     . 

Stroking    downward     from     costal 

Abdominal  muscles  contract  on  side 

Thll  to  LI. 

margin. 

of  stimulus. 

Cremasteric     .    . 

stroking  inner  and  upper   part  of 
thigh.    Or  pressure  over  Hunter's 
canal,  or  over  adductor  tubercle. 

Testicle  is  drawn  up. 

LI  and  L2. 

Gluteal    .... 

Stroking  skin  of  buttock. 

Gluteal  muscles  contract. 

L4  and  L5. 

Plantar   .... 

stroking  sole  of  foot. 

Tensor    fascise    femoris     contracts, 
hallux  and  other  toes  flex,  ankle  is 
dorsi-flexed. 

L5  to  S2. 

Bulbo-Cavernosus 

Pinching  dorsum  of  glans  penis. 

Bulbous  urethra  contracts. 

S3  and  S4. 

Superficial  Anal  . 

Pricking  skin  of  perineum. 

External  anal  sphincter  contracts. 

S4,  S5  and 
Coccygeal. 

The  normal  corneal  reflex  is  a  bilateral  affair,  for,  if  we  touch 
one  cornea,  blinking  occurs  in  bqth  eyes.  Bilateral  loss  of  corneal 
reflexes,  on  stimulating  either  cornea,  occurs  in  coma  from  any 
cause,  including  the  coma  produced  by  general  anaesthetics.  In 
certain  cases  of  hemiplegia  the  corneal  reflex  is  lost  on  the  paralysed 
side,  especially  in  hemiplegias  which  are  associated  with  hemi- 
aneesthesia.  More  commonly  loss  of  the  corneal  reflex  is  due  to 
a  lesion  of  the  reflex  arc,  either  in  its  afferent  (trigeminal  nerve) 
or  its  efferent  limb  (facial  nerve).  In  such  a  case,  in  order  to  decide 
whether  loss  of  the  reflex  is  due  to  affection  of  the  trigeminal  or 
of  the  facial  nerve,  we  note  the  behaviour  of  the  opposite  eye 
when  stimulating  the  cornea  of  the  affected  side.     If  no  blinking 


332  NERVOUS    DISEASES 

occurs  in  the  opposite  eye,  we  have  to  do  with  trigeminal  disease, 
whereas,  if  sensation  is  intact  and  the  facial  nerve  alone  is  paralysed, 
the  contra-lateral  reflex  still  occurs.  Unilateral  loss  or  diminution 
of  the  corneal  reflex  is  often  the  earliest  clinical  sign  of  trigeminal 
paresis,  long  before  any  sensory  loss  can  be  detected.  This  fact 
is  sometimes  of  considerable  value  in  the  diagnosis  of  tumours 
of  the  posterior  cranial  fossa  (see  later,  "  Extra-cerebellar 
Tumours  "). 

Absence  of  the  abdominal  reflex  is  not  uncommon  in  acute 
abdominal  conditions,  notably  in  appendicitis  and  enteric  fever. ^  In 
young  adults  whose  abdominal  walls  are  apparently  normal  and 
in  whom  there  is  no  oedema  or  excessive  obesity,  absence  of  this 
reflex  on  one  or  both  sides  is  strongly  suggestive  of  disseminated 
sclerosis,  as  has  been  pointed  out  by  Striimpell,  E.  Miiller,^  and 


Fig.  173  — Normal  plantar  reflex. 

others.  In  acute  meningitis  the  abdominal  reflexes  tend  to  dis- 
appear early  and  bilaterally.  In  brain  abscess,  however,  with 
commencing  hemiplegic  symptoms,  the  abdominal  reflex  dis- 
appears on  the  hemiplegic  side  only,  as  in  an  ordinary  case  of  recent 
hemiplegia  from  a  vascular  lesion.  Exaggeration  of  the  abdominal 
reflexes  is  fairly  common  during  the  gastric  or  intestinal  crises 
of  tabes,  being  associated  with  cutaneous  hyperaesthesia  of  the 
abdomen. 

Of  all  the  superficial  reflexes,  the  plantar  reflex  is  the  one 
which  has  the  greatest  practical  importance.  In  order  to  test  it, 
the  patient  should  be  lying  down,  his  feet  being  comfortably 
warm.  The  limb  to  be  tested  is  now  partially  flexed  at  the  hip  and 
knee,  and  also  rotated  so  as  to  rest  on  its  outer  side.  Then  with 
some  hard  object  such  as  the  end  of  a  penholder  (applying  light 
pressure,  not  mere  contact),  we  gently  stroke  the  sole  of  the  foot 

^  RoUeston,  Brain,  1906,  p.  99.  ^  Neurologisches  Centralhlatt,  1905,  p.  593. 


REFLEXES  333 

from  behind  forwards,  especially  towards  its  inner  side.  Mean- 
while we  watch  carefully  for  the  first  movement  of  the  great  toe. 
Normally  this  is  a  movement  of  plantar  flexion  (see  Fig.  173). 
The  movement  of  the  other  toes  is  of  less  importance.  It  is  inter- 
esting also  to  note  that,  simultaneously  with  the  toe  movement, 
we  have  a  brisk  contraction  of  the  tensor  fasciae  femoris  (Brissaud's 
reflex),  which  may  occur  even  in  cases  in  which  the  toes  show  no 
movement.  This  shows  that  the  plantar  reflex  is  not  a  phenomenon 
confined  to  the  foot,  but  that  it  implicates  the  whole  lower  limb. 
If  we  employ  a  stimulus  which  is  too  strong,  we  may  have,  in  addi- 
tion, dorsiflexion  of  the  ankle,  and  this  may  obscure  the  toe  move- 
ment. Hence  the  importance  of  a  gentle  stimulus,  graduated  so 
as  just  to  elicit  the  toe  phenomenon  and  no  more. 


Fig.  174. — Babinski's  extensor  plantar  reflex. 

This  normal  plantar  reflex,  flexor  in  tjrpe,  occurs  only  when 
the  reflex  arc  is  intact,  and  when,  in  addition,  the  lower  reflex 
arc  is  in  connection  with  the  cerebral  motor  cortex  by  an  un- 
injured pyramidal  tract.     In  this  sense  it  is  a  "  cortical  "  reflex. 

If  the  pyramidal  tract,  conveying  motor  impulses  downwards 
from  the  cortical  "  leg-centre,"  be  interrupted  in  any  part  of  its 
course  by  injury  or  disease,  or  if  it  be  non-developed,  as  in 
infants  who  have  not  learned  to  walk,  the  type  of  plantar  reflex 
is  different  and  is  known  as  Babinski's  phenomenon,  or  the  extensor 
'plantar  reflex,  whose  spinal  path,  traversing  the  lumbo -sacral 
region,  is  no  longer  controlled  by  pyramidal  impulses.  In 
this  sense  it  is  a  pure  "  spinal "  reflex.  In  the  Babinski  pheno- 
menon, stimulation  of  the  sole,  especially  towards  its  outer  side, 
produces  extension  of  the  hallux  instead  of  flexion  (see  Figs.  173 
and  174).     Dorsiflexion  of  the  hallux  may  be  the  only  visible  effect, 


334  NERVOUS    DISEASES 

but  it  is  never  tlie  only  muscular  contraction.  It  is  always  accom- 
panied by  contraction  of  the  hamstring  muscles,  detected  by 
palpation.  1  Moreover,  this  extensor  movement  of  the  great  toe 
is  slower  than  is  the  normal,  brisk  flexion  response.  Sometimes, 
in  addition  to  extension  of  the  hallux,  we  observe  a  fan-like  spread- 
ing out  of  the  toes — "  phenomene  d'eventail."  An  extensor  plantar 
reflex  is  practically  always  pathological,  except  in  infants  too  young 
to  walk  (gradually  disappearing  after  the  age  of  six  months),  and 
if  constantly  present  it  indicates  an  organic  lesion,  and  one  which 
implicates  the  pyramidal  tract.^  It  is  therefore  of  the  utmost  value 
in  the  diagnosis  between  hysteria  and  organic  disease.  A  bilateral 
extensor  plantar  reflex  may  also  occur  as  a  temporary  phenomenon, 
e.g.  during  post-epileptic  or  ureemic  coma  and  other  transient 
affections  of  the  pyramidal  tract,  often  toxic  in  origin,  such  as 
acute  morphine  poisoning. 

The  extensor  plantar  reflex  can  sometimes  be  elicited  by  other 
devices,  e.g.  by  tapping  with  a  percussion-hammer  over  the  dorsal 
aspect  of  the  metatarso-phalangeal  joint  of  the  big  toe,  just  internal 
to  the  tendon  of  the  extensor  longus  hallucis,^  or  by  sudden,  sharp 
upward  pressure  on  the  sole  of  the  foot,  just  behind  the  ball  of  the 
great  toe,^  or  by  pressure  on  the  deep  flexor  muscles,  as  in  Gordon's  ^ 
paradoxical  flexor  reflex,  which  consists  in  an  extension  movement 
of  the  great  toe  or  of  all  the  toes  when  we  press  deeply,  through  the 
calf  muscles,  between  the  heads  of  the  gastrocnemius,  on  to  the  deep 
flexor  muscles  beneath.  To  elicit  this  reflex,  the  physician  should 
place  himself  on  the  outer  side  of  the  patient's  leg,  the  muscles  of 
which  must  be  completely  relaxed.  This  is  attained  either  by  direct- 
ing the  patient  to  lie  on  his  back  or  making  him  sit  with  his  feet  on 
a  stool. 

Oppenheim's  reflex,  a  contraction  of  the  extensor  longus  hallucis 
and  tibialis  anticus,  is  elicited  in  a  slightly  different  way,  viz.,  by 
firm  stroking  from  above  downwards  with  some  hard  object  (such 
as  the  handle  of  a  percussion-hammer)  just  behind  the  postero- 
internal border  of  the  tibia,  about  the  junction  of  its  middle  and 

^   Walshe,  Brain,  1914,  vol.  xxxvii.  p.  279. 

^  There  is  one  exception  to  this  rule.  This  is  in  the  case  of  a  lower 
motor  neurone  lesion  affecting  the  fiexor  muscles  of  the  toes  and  sparing 
the  extensors.  In  such  a  case  the  only  possible  movement  would  be  ex- 
tension. But  the  other  signs  of  lower  neurone  lesion,  especially  the  electrical 
reactions,  will  prevent  error. 

^  Throckmorton,  Journal  of  American  Med.  Ass.  May  6,  1911. 

*  Tromner,  Deutsche  med.  Wochenschrift,  1911,  No.  37. 

^  Amei-ican  Medicine,  1904,  p.  971, 


REFLEXES  335 

lower  thirds.     Its  significance  is  the  same  as  that  of  Babinski's 
phenomenon. 

The  cremasteric  reflex  is  very  easy  to  eHcit  in  young  children,  by 
stroking  the  inner  side  of  the  thigh.  But  in  old  men  it  is  sluggish 
or  apparently  absent.  Even  in  them,  however,  it  can  usually  be 
elicited  by  sudden  firm  pressure  backwards  against  the  sartorius 
muscle  in  the  region  of  Hunter's  canal,  or  against  the  adductor 
tubercle  of  the  femur ;  this  often  succeeds  when  stroking  the  skin 
in  the  usual  fashion  is  of  no  avail.  Unilateral  absence  of  the 
cremasteric  reflex  occurs  occasionally,  but  not  constantly,  in  organic 
hemiplegia.  The  cremasteric  reflex  is  sometimes  exaggerated  on 
the  affected  side  in  cases  of  sciatic  neuralgia. 

The  bulbo-cavernosus  reflex  is  of  great  diagnostic  value  in 
determining  whether  the  lowest  segments  of  the  spinal  cord  are 
intact  in  a  lesion  about  the  level  of  the  third  sacral  segment — 
where  the  ordinary  reflexes  of  the  lower  limbs  give  us  no  help. 
To  obtain  the  bulbo-cavernosus  reflex,  we  place  one  finger  behind 
the  patient's  scrotum,  pressing  upwards  against  the  bulbous  part 
of  the  urethra.  With  the  other  hand  we  pinch,  or  prick  with 
a  pin,  the  dorsum  of  the  glans  penis  ;  the  bulbous  urethra  is  at 
once  felt  to  give  a  brisk  twitch.  Loss  of  this  reflex  indicates  a 
lesion  somewhere  in  its  reflex  arc,  either  in  the  anterior  cornua 
of  the  third  and  fourth  sacral  segments,  or  in  the  corresponding 
motor  or  sensory  roots  of  the  cauda  equina.  Loss  of  the  bulbo- 
cavernosus  reflex  is  a  fairly  common  sign  in  tabes,  being  due  in 
that  case  to  a  lesion  of  the  afferent  fibres  of  the  reflex  arc. 

The  superficial  anal  reflex  can  be  easily  obtained  by  pricking 
the  skin  of  the  perineum  with  a  long  "  bonnet-pin,"  and  watching 
whether  the  external  sphincter  contracts.  This  reflex  is  sometimes 
lost  in  anaesthesia  of  the  perineum,  or  in  lesions  of  the  fifth  sacral 
or  of  the  coccygeal  segment,  or  of  their  corresponding  motor  roots. 
Organic  hemiplegia  usually  produces,  at  first  at  least,  loss  of 
the  unilateral  superficial  reflexes  all  down  the  paralysed  side,  with 
one  exception — viz.  the  plantar  reflex,  which  persists,  but  from  the 
first  is  changed  into  the  extensor  type.  In  hysterical  hemiplegia, 
on  the  other  hand,  even  though  cutaneous  hemi-anaesthesia  be 
present,  the  unilateral  skin  reflexes  on  the  paralysed  side  are 
usually  preserved,  with  the  exception  of  the  plantar  reflex  which 
is  often  lost.  An  extensor  plantar  reflex  never  occurs  in  pure 
hysteria.     In  hysteria  there  may  be  absence  not  only  of  any  toe 


336 


NERVOUS    DISEASES 


movement  on  stimulation  of  the  sole,  but  there  may  also  be  loss  of 
the  reflex  contraction  of  the  tensor  fasciae  femoris.  This  "  com- 
bined "  absence  of  rej&ex  movement  both  of  the  toes  and  of  the 
fascia  lata  of  the  thigh  is  always  strongly  suggestive  of  hysteria. 
It  is  probably  due  to  a  latent  muscular  spasm. 


Fig.  175. — Method  of  eliciting  jaw-jerk. 

Deep  (Tendon  or  Osseous)  Reflexes.— The  following  table 
gives  a  list  of  those  deep  reflexes  which  we  commonly  study 
when  investigating  cases  of  nervous  disease  : — 


The  knee-jerk  may  be  taken  as  a  type  of  these  tendon  reflexes. 
It  has  been  a  matter  of  dispute  whether  it  is  really  a  true  reflex 


REFLEXES 


337 


or  not.  Strictly  speaking,  the  jerk  occurs  too  soon  after  the  tap 
for  a  nerve  impulse  to  have  time  to  travel  up  to  the  reflex  centre 
in  the  cord  and  down  again  to  the  muscles.  But  so  long  as  the 
reflex  arc  is  intact,  there  is  a  constant  "  reflex  tonus  "  in  the  vastus 
internus  muscle  which,  when  the  tendon  is  struck,  permits  the 
jerk  to  occur.      If  this  reflex  tonus  be  lost  from  interruption  of 


Fig   176. — Iluee-jerk.     Eeinf orcein ent  hj  Jendrassik's  method. 

the  reflex  arc  at  any  point,  the  jerk  can  no  longer  be  obtained. 
Therefore,  for  practical  purposes,  the  knee-jerk,  though  not  a  true 
reflex  action  itself,  is  an  index  of  the  integrity  of  the  reflex  arc. 

To  obtain  the  knee-jerk,  we  feel  for  the  patellar  tendon  and 
strike  it  either  with  the  edge  of  the  hand  or  with  some  other  fairly 
heavy  object,  such  as  a  rubber  percussion-hammer  or  a  heavy 
paper-knife.  The  result  is  a  brisk  contraction  of  the  quadriceps. 
If  we  grasp  the  vastus  internus  with  our  other  hand  we  can  feel 
the   jerk    in   cases  where   it   is  too   feeble   to    move    the    knee- 

Y 


338 


NERVOUS   DISEASES 


joint.  The  knee  must  be  somewhat  bent  to  put  the  quadriceps 
sKghtly  on  the  stretch,  and  the  muscles  must  be  absolutely  re- 
laxed. This  latter  point  is  of  importance ;  for  often  it  happens 
that  a  patient  may  have  his  muscles  in  a  state  of  excessive  spasm, 
so  that  we  may  fail  to  elicit  the  knee-jerk,  and  yet,  if  we  succeed 
in  relaxing  the  muscles  by  passive  movements,  the  knee-jerk  is 


Fig.  177. — Knee-jerk.     Reinforcement  by  Laufenauer's  method. 

not  only  present  but  found  to  be  increased.  The  knee-jerk  in  such 
a  case  is  not  absent,  but  only  "  concealed  "  by  the  spasticity 
of  the  muscles. 

In  testing  the  knee-jerk  the  patient  may  be  sitting  on  a  table 
with  his  legs  dangling  in  the  air,  or  better,  on  a  chair  with  the 
soles  of  the  feet  flat  on  the  ground  and  the  knees  gently  semi- 
flexed, or  one  knee  may  be  crossed  over  the  other.  A  feeble 
jerk  may  be   "  reinforced "   by  Jendrassik's   method   (Eig.   176), 


REFLEXES 


339 


in  which  the  patient  hooks  both  hands  together,  pulling  them 
one  against  the  other,  and  looks  up  towards  the  ceiling,  thereby 
diverting  his  attention  and  relaxing  the  leg  muscles.  A  better 
method  of  reinforcement  is  Laufenauer's,  in  which  we  grasp  the 
patient's  quadriceps  whilst  the  patient  sits  with  liis  soles  flat  on 
the  ground.  The  patient  then  grasps  our  upper  arm  ^vith  one 
hand,  and  suddenly  squeezes  when  told  to  do 
so ;  meanwhile,  down  comes  the  percussion- 
hammer  (Fig.  177).  The  advantage  of  this 
method  is  that  we  can  feel  for  ourselves 
whether  the  patient  is  really  directing  his  atten- 
tion to  the  act  of  reinforcement.  Moreover, 
this  method  can  be  employed  to  reinforce 
feeble  reflexes  of  the  upper  limbs,  whereas 
Jendrassik's  method  is  only  available  for  re- 
flexes of  the  lower  limbs.  Many  other  methods 
of  reinforcement  have  also  been  suggested, 
e.g.  by  making  the  patient  gaze  at  the  ceiling 
and  draw  a  long  breath  (Kronig-^),  or  by 
making  him  read  aloud  from  a 


^£^ 

W 


newspaper  or   book  as   fast   as 
possible  (Rosenbach  ^) . 

Reinforcement  will  make  a 
feeble  jerk  more  evident ;  but 
it  has  no  effect  if  the  jerk  be 
absent. 

The  anJde-jerk  has  a  diag- 
nostic significance  equal  to  that 
of  the  knee-jerk.  To  test  it,  we 
make  the  patient  kneel  on  a 
chair  with  his  feet  projecting 
over  the  edge,  and  then  tap  the 

tendo  Achillis  (Fig.  178) ;  a  brisk  extension  movement  of  the  ankle 
is  the  result.  Some  patients  have  a  difficulty  in  relaxing  the  calf 
muscles  when  kneeling  on  a  chair.  In  such  cases  we  make  the 
patient  stand  with  one  leg  on  the  ground,  resting  his  weight  on  the 
erect  limb,  whilst  the  other  leg  kneels  on  the  chair,  bent  loosely 
to  a  right  angle  at  the  knee.     In  tabes  the  ankle- jerk  is  often  lost 


Fig.  178.— Method  of  eliciting 
ankle-jerk. 


1  Berlin  Idin.  Wochenschrift,  1906,  No.  44. 

2  Miinchener  med.  Wochenschrift,  1907,  No.  2. 


340 


NERVOUS    DISEASES 


before  the  knee-jerk.     In  sciatica  loss  of  tlie  ankle-jerk  indicates 
a  neuritis  as  distinguished  from  a  mere  neuralgia. 

In  the  upper  extremity  we  have  various  deep  reflexes  at  our 
disposal.  Of  these,  the  radial  or  supinator -jerk  is  ordinarily  the 
most  accessible.  In  testing  it,  we  support  the  patient's  forearm 
in  a  semi-supinated  posture,  with  the  elbow  loosely  bent  to  a  right 
angle.  We  tap  with  our  hammer  close  above  the  styloid  process 
of  the  radius  (Fig.  179).  The  supinator  longus  at  once  contracts 
and  with  it  the  other  flexors  of  the  elbow.     Sometimes  the  flexors 


Fig.  179. — Supinator-jerk. 

of  the  fingers  contract  also.  In  health  we  do  not  induce  reflex 
contraction  of  the  finger  flexors  by  themselves.  When  this  occurs — 
so-called  "  inversion  "  of  the  radial  reflex— it  indicates  a  lesion 
at  the  level  of  the  fifth  cervical  segment.  To  elicit  the  triceps- 
jerk,  the  best  way  is  not,  as  stated  in  some  text-books,  to  allow 
the  elbow  to  hang  over  the  back  of  a  chair,  but  rather  to 
support  the  upper  arm  horizontally,  with  the  elbow  loosely  flexed 
at  a  right  angle.  Then,  feeUng  for  the  triceps  tendon,  we  tap 
it  with  our  hammer,  and  the  muscle  at  once  contracts. 

The  pronator  jerk  is  elicited  by  holding  the  forearm  midway 
between  pronation  and  supination,  and  then  tapping  either  on  the 
antero -internal  part  of  the  radius  or  on  the  postero-inf erior  surface 


REFLEXES  341 

of  the  ulna.  This  area  of  the  ulna,  in  certain  subjects,  also  induces, 
in  addition  to  the  pronator- jerk,  a  flexion  movement  of  the  wrist 
and  fingers. 

Loss  of  Deep  Reflexes, — Sometimes  these  reflexes  cannot  be 
ehcited,  even  on  reinforcement.  This  is  almost  always  pathological 
(although  in  very  rare  cases  a  healthy  individual  is  found  to  be 
devoid  of  deep  reflexes),  and  generally  indicates  a  lesion  of  the  reflex 
arc.  If  this  lesion  be  in  the  afferent  limb  of  the  arc,  there  may  also 
be  anaesthesia  of  the  corresponding  nerve-  or  root-area.  If  it  be 
in  the  anterior  cornu,  or  in  the  efferent  motor  path,  there  will  be 
muscular  paralysis,  with  atrophy  of  the  particular  muscle. 

The  following  is  a  list  of  some  of  the  chief  conditions  in  which 
there  is  loss  of  the  deep  reflexes  : — 

Disease.  Site  of  Lesion. 

Neuritis  (Alcohol,  Diabetes,  Diphtheria,  Lead,  Arsenic,   ^ 

VerS^S^^:^Set''^  [  [  l  [  [  ;  Uipheral  nerves,  sensory  or  motor. 
Temporarily  from  compression  by  tourniquet  .        .        .   ) 

Tabes  Dorsalis 

General    Paralysis    of    Insane    (tabetic    type  —  Tabo- 


Friedrefch-f  Ataxia        :::::::■    ^Posterior  columns  of  cord. 


Subacute    Combined    Degeneration    of    Posterior    and 

Lateral  Columns — late  stage  of 

Any  focal  lesion  in  Grey  Matter  of  Cord     ....       Keflex  centre  in  cord. 
Infantile  Paralysis  (Acute  Anterior  Poliomyelitis)    .        .    \ 
Progressive      Muscular     Atrophy     (Chronic      Anterior    I 

An/oU-oThSttal  Sclerosis     :        :        l        !        l        !  interior  cornua  of  cord. 

Syringomyelia I 

Thrombosis  of  Anterior  Spinal  Artery         .         .        .        .  J 

Landry's  Pan] vsis  /Anterior     cornua     and     peripheral 

i^anarj  s  Paralysis ^^     motor  nerves. 

Myopathies  (Pseudohypertrophic  and  Atrophic  types)     .    1  vuscle  itself 

Amyotonia  congenita j  ' 

Family  Periodic  Paralysis  (during  attacks). 
Increased    Intra-Cranial    Pressure    (especially    Hydro- 
cephalus and  Tumours  of  Posterior  Fossa). 
Pneumonia. 

Immediately  after  attack  of  Major  Epilepsy  (post-epileptic  coma). 
Toxic  coma  (urremia,  morphine,  <tc. ). 
During  Spinal  Anaesthesia. 
Complete  transverse  lesion  of  Cord. 

From  this  list  we  see  that,  in  addition  to  permanent  organic 
lesions  within  the  reflex  arc  itself,  there  are  other  conditions  in 
which  the  deep  reflexes  are  aboHshed.  Thus  these  reflexes  are  lost 
in  the  final  stages  of  increased  intra-cranial  pressure,  especially  in 
hydrocephalus  and  in  tumours  of  the  posterior  fossa. 

This  is  attributed  by  Raymond  and  others  to  a  curious  degeneration 
of  the  posterior  spinal  roots,  which  sometimes  occurs  in  such  conditions, 
whereas  van  Gehuchten  ^  ascribes  it  to  loss  of  function  of  the  rubro- 
spinal tracts,  from  pressure  on  the  mesencephalon. 

1  Le  Nevraxe,  1907,  vol.  ix.  p.  39. 


342  NERVOUS   DISEASES 

The  knee-jerks  are  often  lost  during  pneumonia.  In  the  attacks 
of  the  rare  disease  known  as  family  periodic  paralysis  (see  p.  266), 
the  deep  reflexes  in  the  affected  hmbs  are  temporarily  abolished, 
owing  to  temporary  paralysis  of  the  muscle-fibres.  The  deep  jerks 
are  abolished  for  a  few  minutes  just  after  an  epileptic  fit,  during 
the  stage  of  coma  and  flaccidity.  They  may  also  disappear  during 
coma  from  other  causes,  as  in  urgemic  coma  or  in  morphine-poison- 
ing. Spinal  anaesthesia  temporarily  abolishes  all  the  deep  and 
superficial  reflexes  in  the  lower  limbs  (see  p.  448).  As  Babinski 
has  pointed  out,  the  application  of  an  Esmarch  tourniquet,  from 
the  toes  to  the  middle  of  the  thigh,  for  a  period  of  20  to  25 
minutes,  temporarily  abolishes  all  the  reflexes,  deep  and  superficial, 
below  the  level  of  compression,  even  where  there  had  previously 
been  increased  deep  reflexes,  clonus,  and  an  extensor  plantar 
response.  Moreover,  the  plantar  reflex  as  it  returns,  after  removal 
of  the  tourniquet,  may  for  a  few  minutes  show  a  normal  flexor 
response  (especially  on  stimulation  along  the  outer  border  of  the 
foot)  before  the  extensor  response  again  develops. 

We  should  also  remember  that  in  comflete  trans-section 
of  the  spinal  cord,  all  the  deep  reflexes  below  the  level  of 
the  lesion  are  lost.  If,  however,  the  lesion  be  not  complete,  and 
there  still  survives  some  nervous  tissue  connecting  the  upper 
and  lower  portions,  then  the  deep  reflexes  are  exaggerated. 

Exaggeration  of  Deep  Reflexes. — Sometimes  the  deep  reflexes 
are  exaggerated,  so  that  the  slightest  tap  on  the  tendon  produces 
an  abnormally  brisk  contraction.  This  may  be  the  result  of  various 
poisons — e.g.  tetanus,  or  strychnine-poisoning — rendering  the  reflex 
centres  unduly  explosive ;  or  it  may  occur  in  simple  neurasthenia. 
But  organic  lesions  of  the  pyramidal  tract  are  by  far  the  com- 
monest causes  of  permanent  exaggeration  of  the  deep  reflexes.  In 
cases  of  organic  disease,  we  look  also  for  the  presence  of  clonus. 
A  clonus  is  a  rhythmic  series  of  muscular  contractions,  produced 
by  sudden  passive  stretching  of  the  tendon,  the  clonus  continuing 
so  long  as  the  tension  of  the  tendon  is  maintained. 

Clonus  can  be  inhibited  by  pinching  a  large  fold  of  the  skin  of 
the  lower  limb,  especially  of  the  thigh.  This  stops  the  clonus  at 
once. 

Ankle-clonus  is  the  commonest  clinical  variety  of  clonus.  To 
elicit  it,  the  knee  is  passively  flexed  (the  angle  of  flexion  varying 
in  diflterent  cases),  and  the  ankle  is  suddenly  dorsiflexed  by  upward 


REFLEXES 


343 


pressure  on  the  sole  of  the  foot  (Fig.  180).  Ankle-clonus  is  due, 
as  Weir-Mitchell  has  pointed  out,  to  contraction,  not  of  the 
gastrocnemius  but  of  the  soleus  muscle,  since  the  position  of  the 
knee  which  is  best  for  ehciting  ankle-clonus  is  one  in  which  the 
gastrocnemius  is  relaxed. 

A  spurious  ankle-clonus  is  sometimes  obtained  in  cases  of  hysteria. 
This  can  usually  be  distinguished  from  genuine  clonus  by  a  char- 


FlG.  180. — Method  of  eliciting  ankle-clonus. 

acteristic  feeling  as  of  voluntary  contraction  in  the  muscles,  espe- 
cially at  the  commencement  of  the  clonus,  difficult  to  describe 
in  words.  Spurious  clonus  is  generally  poorly  sustained  and  often 
irregular  in  rhythm.  It  is  never  associated  with  an  extensor 
plantar  reflex. 

Knee-clonus  or  rectus-clonus  is  best  obtained  by  sudden  down- 
ward traction  on  the  patella,  the  knee  being  passively  extended. 


344  NERVOUS   DISEASES 

In  chronic  organic  affections  of  the  pyramidal  tract,  practically 
every  one  of  the  deep  jerks  may  become  exaggerated  into  clonus. 
Thus  in  advanced  disseminated  sclerosis  we  may  find  in  the  same 
patient  jaw-clonus,  elbow-clonus,  wrist-clonus,  finger-clonus,  knee- 
clonus,  ankle-clonus,  toe-clonus,  &c. 

The  presence  of  true  clonus  indicates  that  the  reflex  arc  is 
hyper-excitable,  owing  to  withdrawal  of  the  regulating  or  restrain- 
ing influence  normally  exerted  through  the  pyramidal  tract.  Ex- 
aggeration of  the  deep  reflexes  is  therefore  one  of  the  cardinal  signs 
of  a  chronic  lesion  of  the  upper  or  cortico-spinal  motor  neurone. 

Bechterew  and  MendeVs  rejlex  is  elicited  by  tapping  the  dorsum 
of  the  foot,  preferably  over  the  cuboid  bone.  Instead  of  the 
normal  extension  of  the  four  outer  toes,  due  to  stimulation  of  the 
extensor  brevis  digitorum,  we  have  a  flexor  movement  of  these 
toes.  This  phenomenon  only  occurs  in  organic  lesions  of  the 
pyramidal  tract.  Rossolimo^s  sign  of  pyramidal  disease  consists 
in  a  sudden  flexion  movement  of  the  toes,  produced  by  their  previous 
extension,  e.g.  by  striking  on  their  plantar  surface. 

In  the  upper  limb  Tromner's  ftnger-phenomenon  ^  of  pyramidal 
disease  is  elicited  by  lightly  grasping  the  patient's  semi-pronated 
hand  and  then  Ughtly  flicking  the  terminal  phalanx  of  the  index 
finger  in  a  palmar  direction.  In  health,  the  patient's  thumb  remains 
motionless,  but  in  disease  of  the  pyramidal  fibres  of  the  upper 
Hmb  the  thumb  makes  a  reflex  movement  of  adduction.  A  similar 
movement  can  also  be  elicited  by  firm,  slow  scratching  along  the 
ulnar  side  of  the  palm,  from  the  base  of  the  little  finger  towards 
the  pisiform  bone,  or  inversely.^ 

It  is  unnecessary  to  give  a  list  of  the  various  organic  diseases 
in  which  the  deep  reflexes  are  exaggerated.  Suffice  it  to  say  that 
any  chronic  lesion  of  the  pyramidal  tract  will  produce  exaggeration 
of  the  deep  reflexes  below  the  level  of  the  lesion.  Thus  in 
paraplegia  due  to  myelitis,  to  lateral  sclerosis,  or  to  some  other 
affection  of  the  lateral  columns,  or  in  hemiplegia  from  organic 
brain  disease,  ithere  is  exaggeration  of  the  deep  reflexes  in  the 
paralysed  hmbs,  owing  to  injury  or  disease  of  the  pyramidal  fibres. 

There  is  an  important  exception  to  this  rule,  to  which  we 
have  already  referred,  namely  in  total  trans-section  of  the  spinal 
cord,  as  in  some  cases  of  bullet-wound  or  of  fractured  spine.     Such 

1  Neurologlsches  Centralhlatt,  1932,  p.  603. 

^  Marie  and  Foix,  Revue  neurologique,  1915,  p.  583. 


REFLEXES  345 

total  lesion  produces  a  permanent  flaccid  paralysis  of  the  lower 
limbs,  with  loss  of  the  deep  reflexes  (Bastian's  law).  But  if  the 
lesion  be  incomplete,  we  have  the  usual  spastic  type  of  paraplegia, 
with  increased  deep  reflexes.  In  both  instances,  whether  the  lesion 
be  total  or  partial,  we  have  the  reflexes  of  spinal  automatism  in 
the  lower  limbs,  and  usually  an  extensor  type  of  plantar  reflex. 
In  some  total  transverse  lesions,  however,  the  plantar  reflex  may 
be  flexor  in  type,  temporarily  or  permanently. ^ 

We  should  also  mention  that  in  the  early  stages  of  a  peripheral 
neuritis,  e.g.  in  localised  neuritic  atrophy  in  association  with  arthritis, 
the  deep  reflexes  may  be  exaggerated.  But  this  soon  passes  off 
and  is  succeeded  by  their  diminution  and  loss.  Again,  in  subacute 
combined  degeneration  of  the  lateral  and  posterior  columns  of  the 
cord,  there  is  an  early  stage  of  spasticity  with  increased  deep 
reflexes,  and  a  terminal  stage  of  flaccid  paralysis  with  loss  of 
reflexes. 

Sometimes  in  the  flexed  type  of  spastic  paraplegia  (see  p.  286) 
the  muscular  rigidity  of  the  paralysed  Umbs  is  so  excessive  that  it 
may  be  impossible  to  obtain  the  knee-jerks  and  ankle- jerks,  which 
we  should  expect  to  find  exaggerated  in  these  cases.  This  is 
because  the  muscles  are  already  in  a  state  of  tonic  spasm.  But 
if  we  succeed  in  temporarily  relaxing  them,  by  passive  changes 
of  posture,  we  can  sometimes  obtain  the  increased  jerks  and  even 
the  clonus.  In  most  cases,  the  spasticity  and  the  presence  of 
an  extensor  plantar  reflex  will  prevent  errors  in  diagnosis. 

Pupillary  Light  Reflex. — This  occupies  a  special  category  of  its 
own.  The  reflex  is  elicited  by  exposing  the  pupil  to  light,  after 
previous  shading.  Normally  under  such  conditions  the  pupil 
contracts  briskly,  both  when  stimulated  directly  and  when  the 
pupil  of  the  opposite  eye  is  exposed  to  Ught  (consensual  reflex). 
In  some  respects  the  pupil  reflex  to  light,  although  occurring  in  a 
non-striated  muscle,  is  analogous  to  a  deep  reflex,  and  it  is  useful 
to  remember  that  in  tabes  this  reflex  disappears,  as  do  the  ordinary 
tendon-reflexes.  But  the  subject  of  the  various  pupil-reflexes  and 
their  connections  with  the  third  nerve,  with  the  ciliary  ganglion, 
and  with  the  cervical  sympathetic  is  discussed  elsewhere  (see 
"  Cranial  Nerves,"  p.  137,  and  "  Cervical  Sympathetic,"  p.  359). 

Organic  Motor    Reflexes. — These    are    concerned   with   the 

^  Dejerini  et  Mouzon,  Revue  neurologique,  1915,  p.  155, 
Barre,  ibid.,  1915,  p.  667. 


346 


NERVOUS    DISEASES 


vegetative  nervous  system  and  with  the  contraction  of  non- 
striated,  involuntary  muscles.  The  contraction  of  non-striated  or 
smooth  muscles  is  slow,  unlike  the  brisk  twitch  of  a  reflex  in  a 
striated  muscle.  The  following  is  a  list  of  organic  reflexes  which  are 
of  diagnostic  interest.  In  some  of  these,  such  as  the  cilio-spinal 
or  the  scrotal,  the  reflex  movement  is  executed  entirely  by  non- 
striated  muscle.  In  others,  such  as  the  vesical,  uterine,  or  rectal, 
the  non-striated  muscle  is  reinforced  by  voluntary  striated  muscles. 


Method  of  Eliciting. 

Result. 

Cilio-spinal    .    . 
Oculo-cardiac    . 

Cutaneo-gastric 
Scrotal      .     .     . 

Vesical      .     .    . 

Rectal  .... 

Genital      .     .     . 
ITterine     .     .     . 
Internal  anal     . 

Pinching  or  scratching  skin  of  neck. 

Firm  compression  of  eyeball. 

Light  stroking  along  left  costal  margin. 

Repeated  stroking  of  perineum  or  ap- 
plication of  cold. 

Distension  or  irritation  of  bladder  or 
posterior  urethra. 

Distension  or  irritation  of  upper  part 
of  rectum. 

From  cerebrum  or  periphery. 

Distension  or  stimulation  of  uterus. 

Distension  of  anus  by  finger. 

Pupil  dilates. 
Slowing  of  heart. 
Stomach  contracts. 
Dartos  contracts. 

Bladder-wall  contracts. 

Rectum  contracts. 

Erection  of  corpora  cavernosa. 

Uterus  contracts. 

Internal  sphincter  ani  contracts. 

In  many  of  these  the  reflex  movement  can  be  accomplished,  more 
or  less  perfectly,  independently  of  the  central  nervous  system. 

The  oculo-cardiac  reflex  is  elicited  by  firm  compression  of  the 
eyeballs  backwards  into  the  orbits.  In  most  normal  individuals  this 
produces  an  immediate  slowing  of  the  cardiac  rhythm,  amounting 
to  six  or  eight  beats  per  minute.  The  slowing  ceases,  immediately 
the  compression  is  discontinued.  The  afferent  path  of  this  reflex 
is  in  the  trigeminal  nerve ;  its  efferent  path  is  in  the  autonomic 
fibres  of  the  vagus.  The  oculo-cardiac  reflex  is  specially  well 
marked  in  the  "  vago-tonic  "  type  of  individual,  whereas  in  "  sym- 
pathetico-tonic  "  individuals  it  may  be  diminished  or  absent.  It 
is  sometimes  exaggerated  in  exophthalmic  goitre  and  frequently  lost 
in  tabes.  It  can  be  temporarily  abohshed  by  the  administration 
of  atropin. 

The  cutaneo-gastric  reflex,  to  which  attention  has  been  specially 
directed  by  Percy  Mitchell, ^  is  of  considerable  clinical  interest.  It  is 
elicited  by  laying  the  patient  flat  on  his  back  and  gently  stroking 
the  skin  along  the  left  costal  margin,  beginning  about  the  tenth 
costal  cartilage,  gradually  ascending  towards  the  xiphisternum, 
and  descending  slightly  down  the  right  costal  arch.     Meanwhile  a 

1  Lancet,  Jan.  28,  1911. 


REFLEXES  347 

fairly  heavy  phonendoscope  is  placed  on  the  epigastrium,  whereby 
the  observer  can  hear  the  movement  of  stomach-contents,  gas,  or 
air,  as  each  wave  of  reflex  contraction  passes  along  the  stomach 
wall  from  left  to  right.  After  a  few  seconds  or  minutes  of  stroking, 
we  hear  bubbles  of  gas  being  expelled  through  the  pylorus.  We 
cease  our  stroking  until  that  particular  contraction  comes  to  an 
end,  then  proceed  again,  until  by  successive  contractions  the  gas 
is  all  expelled.  On  continuing  further  strokings,  we  hear  low, 
crunching  sounds,  "  like  a  man  walking  on  frozen  snow,"  probably 
due  to  churning  movements  of  the  pyloric  antrum.  This  sound 
increases  in  intensity  as  the  muscular  wave  approaches  the  pylorus. 
When  the  pylorus  opens,  a  sizzling  and  gushing  sound  is  heard,  as 
the  fluid  passes  through  the  pylorus.  Towards  the  end  of  the 
seance  we  sometimes  hear  a  long-continued  powerful  rush  of  fluid — 
a  debacle,  when  the  stomach  completely  empties  itself  into  the 
duodenum.  When  the  stomach  is  at  last  empty,  stimulation 
produces  a  soft,  sighing  sound,  apparently  due  to  peristalsis  of 
the  empty  organ. 

This  reflex  is  of  value  in  the  treatment  of  atonic  dilatation 
of  the  stomach.  Before  attempting  to  elicit  the  reflex,  an  interval 
of  three  or  four  hours  should  be  allowed  to  elapse,  after  the  pre- 
ceding meal,  in  order  to  allow  time  for  gastric  digestion  to  be  com- 
plete. 

In  some  text-books  the  statement  is  made  that  the  reflex 
centres  for  the  bladder,  uterus,  and  rectum  are  situated  within 
the  cord.  But  clinical  and  pathological  evidence,  notably  by 
L.  R.  Miiller,^  has  shown  that  the  lowest  reflex  centres  for  the 
contraction  of  the  bladder,  and  of  the  neighbouring  hollow  viscera 
possessing  non-striated  muscular  walls,  are  situated  extra-spinally, 
in  the  hypogastric  and  hsemorrhoidal  plexuses  of  the  vegetative 
nervous  system. 

The  autonomic  vesical  centre  can  be  stimulated  from  the 
cerebio-spinal  system.  Micturition  in  the  adult  is  a  voluntary 
act,  but  only  to  this  extent  that  it  can  be  voluntarily  initiated. 
This  is  accomphshed  by  contracting  the  diaphragm  and  abdominal 
walls,  producing  a  rise  in  the  intra-vesical  tension,  which  starts 
the  reflex ;  meanwhile  the  striated  constrictor  urethrse  is 
voluntarily  relaxed.  But  the  non-striated  bladder-wall  itself,  the 
so-called  detrusor  urinae,  is  not  under  control  of  the  will.     Once 

'   Deutsche  Zeitschrift  ficr  Nervenheilkunde,  1901,  Band  21,  s.  86. 


348  NERVOUS    DISP^ASES 

started,  the  bladder  empties  itself  spontaneously,  and  we  can  stop 
the  act  only  by  forcibly  innervating  the  constrictor  urethrse, 
usually  a  matter  of  considerable  effort.  But  reflex  micturition 
is  often  excited  by  irritation  of  the  urethra,  especially  of  its 
vesical  end.  Thus  if  a  few  drops  of  urine  trickle  into  the 
prostatic  urethra,  an  imperious  reflex  act  of  micturition  results, 
which  is  difiicult  to  prevent.  Similar  phenomena  are  produced  by 
the  irritation  of  a  posterior  urethritis. 

The  fibres  from  the  brain  and  spinal  cord  to  the  sacral  autonomic 
vesical  centre  reach  it  through  the  lowest  spinal  roots,  from  the 
third  to  the  fifth  sacral,  so  that  lesions  of  the  spinal  cord  or  cauda 
equina  constantly  cause  bladder  trouble.  This  generally  takes  the 
form  of  initial  retention  of  urine,  followed  after  several  days  by  in- 
termittent reflex  incontinence  ("  incontinenza  a  getto  "  of  Itahan 
writers  i),  in  which  the  bladder  contracts  intermittently  and  expels 
the  urine  at  intervals.  Such  reflex  incontinence  is  generally  associ- 
ated with  incomplete  emptying,  so  that  a  certain  amount  of 
"  residual  urine  "  remains  in  the  bladder.  In  cases  of  coma  or  of  the 
deep  insensibihty  of  fevers  such  as  typhoid,  we  observe  an  initial  re- 
tention of  urine,  followed  by  distension,  paralysis  of  the  bladder- wall 
and  overflow  dribbling  ("  incontinenza  'per  regurgito  "). 

The  sensory  nerves  from  the  bladder  pass  through  the  sacral 
autonomic  by  the  rami  communicantes,  and  along  the  posterior  roots 
into  the  spinal  cord.  They  serve  to  inform  us  of  the  distension 
of  the  bladder.  There  are  also  higher  micturition  centres,  some  in 
the  spinal  cord  (in  the  lower  sacral  segments) ,  others  higher  still  in 
the  mid-brain,  in  the  corpus  striatum  and  optic  thalamus  ;  others, 
highest  of  all,  in  the  motor  cortex,  between  the  arm  and  leg  centres, 
controlling  the  sub-cortical  and  spinal  centres.  When  these 
higher  centres,  spinal  or  cerebral,  are  hyper-excitable,  whether 
from  disease  or  from  emotion,  we  may  have  precipitancy  of 
micturition,  or  even  enuresis,  a  condition  in  which  the  brain  and 
spinal  cord  on  the  slightest  provocation  send  impulses  which  relax 
the  compressor  urethrse.  A  similar  condition  exists  in  infants 
who  have  not  learned  to  control  their  subcortical  micturition 
centres. 

True  dribbling  of  urine  ("  incontinenza  vera  "),  as  distinguished 
from  intermittent  contraction  of  the  bladder,  occurs  most  typically 
in  cases  of  tabes  and  is  mainly  due  to  ansesthesia  of  the  bladder, 

^  Rebizzi,  Rivista  di  Patologia  Nervosa  e  Mentale,  1905,  p.  80. 


REFLEXES  349 

which  being  now  insensitive  to  distension,  is  no  longer  stimulated 
to  contract  by  the  normal  accumulation  of  urine.  The  tabetic 
patient  with  an  anaesthetic  distended  bladder  expels  his  urine,  not 
by  contraction  of  the  bladder  but  by  pressure  with  his  abdominal 
walls.  This  can  readily  be  verified  if  we  have  to  pass  a  catheter 
for  the  purpose  of  emptying  a  tabetic  patient's  bladder.  True 
dribbling  also  occurs  in  an  over-distended  bladder  which,  from 
obstruction  in  the  prostate  or  urethra,  has  become  flaccid,  paralysed 
and  atonic. 

The  internal  anal  reflex  is  tested  by  inserting  a  finger  within 
the  anus.  Normally  the  finger  is  tightly  grasped  by  the  non- 
striated  internal  sphincter,  innervated  by  sacral  autonomic  fibres. 
This  reflex  is  independent  of  the  superficial  anal  reflex  of  spinal 
origin,  to  which  we  have  already  referred.  When  the  internal 
anal  reflex  is  lost,  the  anus  no  longer  grasps  the  finger  but  remains 
open  for  several  seconds,  "  yawning,"  after  the  finger  has  been 
withdrawn.  Such  loss  is  most  commonly  due  to  anaesthesia  of 
the  anus,  as  in  tabetic  or  other  lesions  of  the  cauda  equina.  The 
result  is  incontinence  of  faeces.  If  there  be  a  lesion  within  the 
spinal  cord,  above  the  spinal  centre  in  the  conus  medullaris,  there 
is  intermittent  rectal  incontinence.  But  if  the  lesion  be  in  the 
afferent  nerves  from  the  rectum,  the  internal  sphincter  loses  its 
reflex  tonus  and  remains  relaxed,  and  the  faeces,  if  fluid,  dribble 
away  continuously  when  they  enter  the  anaesthetic  rectum,  the 
patient  being  unconscious  of  the  fact. 

To  test  the  scrotal  reflex,  which  is  an  excellent  example  of  a 
purely  autonomic  motor  phenomenon,  the  patient  stands  bend- 
ing forwards  with  his  legs  wide  spread  and  scrotum  hanging  free. 
The  skin  of  the  perineum  is  now  stroked  with  some  hard  object 
five  or  six  times  in  succession.  After  a  few  seconds  an  extremely 
slow,  worm-like  contraction  appears  in  the  non-striated  dartos 
muscle,  beginning  near  the  perineal  part  of  the  scrotum  and 
spreading  forwards.  This  reflex  can  also  be  ehcited  by  the  apphca- 
tion  of  cold  to  the  perineum  or  scrotum. 

In  addition  to  the  foregoing  ordinary,  innate,  or  stereotj^ed 
reflexes,  which  in  normal  individuals  traverse  relatively  simple 
paths,  the  central  nervous  system  also  possesses  the  faculty  of  estab- 
lishing new  or  acquired  reflexes  by  a  process  of  practice  and  repeti- 
tion. These  so-called  conditional  reflexes  have  been  specially 
studied  by  Pawlow  and  his  school.     For  example,  the  secretion 


350  NERVOUS    DISEASES 

of  saliva  can  be  induced  as  an  ordinary  reflex  in  an  untrained  animal 
by  the  introduction  of  food  or  of  acid  substances  into  tbe  mouth. 
Other  afferent  stimuli  can  also  induce  reflex  salivation,  e.g.  the  sight 
or  smell  of  food,  and  sometimes  even  the  thought  of  food.  More- 
over, stimuli  of  an  entirely  extraneous  and  indifferent  nature,  by 
a  process  of  training,  can  also  be  made  to  induce  salivary  secretion, 
thereby  constituting  a  new  or  acquired  reflex.  Thus  in  the  case 
of  a  dog,  if  a  certain  note  be  struck  on  a  gong  on  every  occasion 
immediately  before  food  is  placed  in  the  animal's  mouth  (or  if  in 
another  dog  a  painful  electrical  stimulus  be  applied  to  the  skin 
within  a  few  seconds  prior  to  administering  food),  then  in  the  course 
of  time,  by  a  process  of  repetition  of  the  same  experiment,  the 
central  nervous  system  comes  in  the  one  animal  to  associate  the 
sound  of  the  gong,  and  in  the  other  animal  to  associate  the  painful 
electrical  stimulus,  with  the  administration  of  food  and  with  its  con- 
comitant salivary  secretion.  Finally,  after  a  time,  the  "  conditional 
stimulus  "  alone  suffices,  even  without  the  administration  of  food, 
to  induce  salivation,  so  that  in  the  one  animal  the  mere  sound  of 
the  gong,  or  in  the  other  the  mere  application  of  a  painful  electrical 
stimulus  to  the  skin,  at  once  induces  copious  salivation  without 
producing  the  ordinary  and  natural  reflex  of  fright  or  pain  to  which 
these  stimuli  originally  gave  rise.  In  other  words,  the  stimulus 
has  been  diverted  from  one  part  of  the  nervous  system  to  another. 
These  are  "  conditional  "  or  acquired  reflexes,  which  are  established 
by  means  of  specialised  "  analysors "  comprising  the  peripheral 
end-organ  of  the  sense-organ  (hearing,  pain,  &c.),  the  corresponding 
afferent  nerve-fibre,  and  its  ultimate  termination  in  the  sensory 
cortex.  Such  analysors  are  constantly  at  work  regulating  the  re- 
actions of  the  living  organism  to  its  varying  environment.  Condi- 
tional reflexes  are  the  cause  of  many  psycho-motor  and  other  pheno- 
mena of  which  familiar  examples  can  be  found.  The  maxim  that 
"  practice  makes  perfect  "  is  based  on  the  fact  that  complex  psycho- 
motor actions,  originally  demanding  a  considerable  effort  of  conscious 
attention  {e.g.  swimming,  riding,  &c.),  may  in  the  course  of  time 
become  conditional  reflexes,  so  that  the  individual,  whilst  perform- 
ing them,  becomes  able  at  the  same  time  to  direct  his  conscious 
attention  to  other  things. 


CHAPTER   XX 

AFFECTIONS   OF   THE  VEGETATIVE   NERVOUS  SYSTEM 

The  Vegetative  Nervous  System  innervates  the  non-striped 
muscles  of  the  body  generally,  also  the  pupils,  the  various  glands 
and  viscera,  the  heart  and  blood-vessels,  and  the  genital  organs. 
It  is  developed  by  outgrowth  from  the  cerebro- spinal  system,  with 
which  it  remains  connected  by  afferent  and  efferent  fibres.  More- 
over, a  number  of  specialised  vegetative  nerve-cells  remain  within 
the  cerebro-spinal  axis,  thereby  accounting  for  the  occurrence  of 
vegetative  phenomena  in  certain  central  diseases.  Unlike  the 
nerves  of  the  cerebro-spinal  system,  which  pass  directly  from  the 
nerve-cells  of  the  lower  neurons  to  the  voluntary  muscle-fibres 
which  they  innervate,  no  fibre  of  the  vegetative  system  passes 
from  the  cerebro-spinal  axis  to  an  involuntary  end-organ  without 
the  interposition  of  a  ganglion-cell  in  its  course.  The  nerve-fibres 
passing  from,  the  cerebro-spinal  cells  to  the  ganglion-cells  are  termed 
pre-ganglionic ;  those  passing  from  the  ganglion-cells  to  the  viscera 
are  post-ganglionic. 

The  vegetative  system  has  two  great  subdivisions — the  sym- 
pathetic system  proper  and  the  autonomic  or  para-sympathetic 
system.  These  two  divisions  are  not  only  anatomically  distinct, 
but  also  physiologically  antagonistic,  mutually  counterbalancing 
one  another. 

The  sympathetic  proper  consists  of  two  chains  of  gangliated  cords, 
like  two  strings  of  beads,  one  on  each  side,  close  in  front  of  the  vertebral 
column,  from  the  base  of  the  skull  to  the  front  of  the  coccyx.  In  the 
thoracic,  lumbar,  and  sacral  regions  the  sympathetic  ganglia  correspond 
in  number  to  the  spinal  nerve-roots,  but  in  the  neck,  instead  of  eight 
ganglia  there  are  only  three  in  each  chain — superior,  middle,  and 
inferior.  These  cervical  ganglia  are  connected  with  the  spinal  cord, 
not  through  the  cervical  roots,  but  through  the  first  and  second  thoracic 
roots  (see  later,  p.  357).  Each  chain  is  made  up  of  multipolar  nerve- 
cells  with  nerve-fibres,  all  of  them  involuntary,  destined  for  gland- 
tissue,  for  blood-vessels,  and  for  organs  which  possess  non-striped 
muscle-fibres.  The  sympathetic  chain  is  connected  with  the  spinal 
cord  by  short  rami  communicantes,  some  of  them  white,  some  of  them 
grey  (see  Fig.  181).  The  white  rami,  composed  of  very  fine  meduUated 
fibres,  are  efferent  (viscero-motor)  or  spino-sympathetic.  They  are 
pre-ganglionic  fibres,  arising  from  special  cells  in  the  interniedio-lateral 

351 


352 


NERVOUS    DISEASES 


region  (nucleus  sympatheticus)  of  the  spinal  cord.  They  emerge  from 
the  cord  through  the  anterior  roots,  commencing  with  the  first  thoracic, 
and  join  the  corresponding  sympathetic  ganglia.     The  qrey  rami  pass 


OIL/\TOR     PUP/LL/E 
IPHIfJCTER      fUPILL/E 
CILIARy    MUSCLE 
NON-^rniPED  LEyy^TOK 
OtBir/iL.    ffLfSCUE. 


BL  OOD  y£S5E-LS    OF  NOSE , 
PH/^KVU^     4    MOUTH 
HON -STRIPED  MUSCLE  OF 
INTESTINAL   C/IN^L  FfiOM 
MOUTH  TO  OESCENDINQ 
COLON. 

NON-.STRIPEJ>  MUSCLES  OF 
Tlt/^CHEy^    /  BRONCHI 
C/iRDIO  -INHIBITORY 
C/^HD/O  -^CCEL  EK/I  TOR. 
BRONCHO    ff/l-i^TOR. 
Gj^STK/C    SL-^NDS. 
LIVER      P^HCR.EFI3 
/iRTERIZS    MUSCl.ES    ^- 
GL^NDS    OF   SKIN 
BLOODyESSELS  OF 
INTESTINAL  C^N/tl    FROM 
MOUTH      ro    RECTUM 
PULMON/^KT  If.  /9BDOMINy9L 
BLOODi'ESSELS 
/iPTERIES    OFSKELET^L 
MUSCLEJ.     VON-STR/PED 
MUSCLE  OF  SPLEEN,  URETER. 
JflNTERHi^l   (iEN/T/IL  Oft<;/^HS 
MUSCLE.    OP  OESCEHDINa 
COLON     RECTUn      #• 
^N/iL     C/iNAL 
MUSCLt  OF  BLADDER.- WALL 
CORPORA    C^yERNOSA 
y/ISO-COHSTRICTOR    OF 
EXTERNAL     GENITALS 
y/iSO    DILATOR    OF 
EXTERM/tL    GENITALS) 


'.'.y.\'l'y.\::^';'<AHfD-&li/^lfi     AUTONOMIC 


Fig  181. — Tlie  Vegetative  Nervous  Svstem,  wilh  its  autonomic  and  sympathetic 
subdivisions.  In  the  sympathetic,  each  nerve  cell  (S)  has  an  adrenal  secretory 
cell  (A)  in  connection  with  it. 

from  the  sympathetic  to  the  cerebro-spinal  nerves.  Some  of  these 
fibres  are  medullated,  afferent  (viscero-sensory)  in  function,  and  belong 
to  the  cells  of  the  posterior  root  ganglia  ;   most  of  the  fibres  are  non- 


AFFECTIONS  OF  VEGETATIVE  NERVOUS  SYSTEM     353 

meduUated,  originating  in  the  sympathetic  ganglia  (post-ganglionic 
fibres),  and  passing  by  the  grey  rami  to  the  spinal  nerves,  in  which  they 
are  conducted  to  their  destinations,  supplying  involuntary  efferent 
fibres  to  the  periphery,  their  functions  being  viscero-motor,  vaso-motor, 
vaso-inhibitory,  pilo-motor,  secretory,  &c. 

The  autonomic  system  (or  system  of  the  "  extended  vagus  ")  does 
not  form  a  chain  like  the  sympathetic  proper,  but  consists  of  nerve- 
fibres  with  ganglia  placed  more  peripherally.  They  also  have  their 
corresponding   white   rami.     Some   come   from   higher  levels   {cranio- 


FiG.  182 


cervical  autonomic),  either  from  the  mid-brain  (along  the  oculo-motor 
nerve  to  the  ciliary  ganglion,  and  thence  to  the  iris  and  ciliary  muscle) 
or  from  the  medulla  (along  the  nervus  intermedins,  giosso-pharyngeal, 
and  vagus  to  various  ganglia— spheno-palatine,  otic,  and  sub -maxillary). 
These  white  rami  have  their  cells  of  origin  in  special  nuclei  in  the 
brain-stem  (E dinger- Westphal  nucleus  in  the  mid-brain,  and  nucleus 
lateralis  in  the  bulb),  which  are  homologous  with  the  intermedio- 
lateral  nucleus  in  the  spinal  cord.  The  vagus  nerve  is  the  largest  and 
most  important  constituent  of  the  cranio-cervical  autonomic  system. 
Other  autonomic  fibres  {sacral  autonomic)  emerge  from  the  spinal  cord 
at  a  level  lower  than  that  of  the  sympathetic  proper,  viz.  through  the 
second,  third,  and  fourth  sacral  nerves  (see  Fig.  181),  and  supply  the 

z 


354  NERVOUS    DISEASES 

descending  colon,  sigmoid,  rectum,  bladder,  urethra,  and  genital 
organs. 

The  vegetative  system  has  three  great-  fre-vertebral  plexuses — the 
cardiac,  the  solar  (or  abdominal  aortic),  and  the  hypogastric.  These 
plexuses  are  all  situated  mesially,  and  they  receive  branches  from  the 
cerebro-spinal  nerves  as  well  as  from  the  sympathetic  chains. 

The  cardiac  plexus,  receiving  autonomic  fibres  from  the  vagi  and 
sympathetic  fibres  from  all  of  the  cervical  gangia,  has  a  superficial 
and  a  deep  division.  The  superficial  cardiac  plexus  is  situated  in  the 
concavity  of  the  aortic  arch  ;  the  deep  division,  much  larger,  lies  behind 
the  aortic  arch,  between  it  and  the  trachea.  From  these  two  divisions 
fibres  pass  on  to  the  coronary  and  pulmonary  plexuses. 

The  solar  (or  abdominal  aortic)  plexus  lies  in  front  of  the  upper 
part  of  the  abdominal  aorta  and  of  the  pillars  of  the  diaphragm.  It 
receives  autonomic  fibres  from  the  vagi,  and  sympathetic  fibres  from 
the  greater  and  lesser  splanchnic  nerves,  derived  from  the  thoracic 
part  of  the  gangliated  chains.  The  solar  plexus  gives  off  numerous 
branches  forming  subsidiary  plexuses  around  various  branches  of  the 
abdominal  aorta. 

The  hypogastric  plexus,  which  supplies  the  pelvic  viscera,  lies  in 
the  space  between  the  two  common  iliac  arteries.  It  receives  sym- 
pathetic fibres  from  the  lumbar  ganglia,  and,  after  dividing  into  the 
two  pelvic  plexuses,  one  on  each  side  of  the  rectum,  or  vagina,  receives 
sacral  autonomic  fibres  from  the  third  and  fourth  sacral  nerves.  The 
pelvic  plexuses  subdivide  and  supply  the  rectum,  bladder,  and  genital 
organs. 

There  are  two  main  classes  of  reflexes  within  the  vegetative 
nervous  system.  In  one  variety  the  centripetal  path  runs  in  a 
cerebro-spinal  nerve,  and  the  stimulus,  on  reaching  the  brain-stem, 
is  reflected  outwards  along  a  fibre  of  the  vegetative  system.  Ex- 
amples of  this  class  of  reflex  are  salivation,  sweating,  flushing  of 
the  skin,  the  genital  reflex,  &c.  A  second  variety  of  vegetative 
reflex  has  both  its  afferent  and  its  efferent  limb  running  in  vege- 
tative paths,  e.g.  the  ordinary  movements  of  hollow  organs  (such 
as  the  gastro -intestinal  tract,  uterus,  ureter,  or  bladder),  all  of  which 
contract  independently  .of  cerebro-spinal  stimuli.  The  cutaneous 
and  internal  organs,  containing  non-striped  muscle  or  secretory 
cells,  are  independent  of  our  will.  Nevertheless  they  can  be  pro- 
foundly influenced  by  the  central  nervous  system  through  emotional 
stimuli  such  as  anger,  fear,  pleasure,  surprise,  shame,  sexual  excite- 
ment, &c. 

With  regard  to  the  vegetative  afferent  fibres  in  the  grey  rami, 
it  is  well  recognised  that  the  viscera  have  a  sensibility  of  their  own, 
and  are  the  starting-point  of  impulses  which,  like  other  sensory 


AFFECTIONS  OF  VEGETATIVE  NERVOUS  SYSTEM     355 

stimuli,  are  conveyed  to  the  spinal  cord  along  the  posterior  roots. 
Normally  these  visceral  stimuli  do  not  reach  our  consciousness,  so 
that  in  health  we  are  unaware  of  the  functional  activity  of  our 
organs,  except  for  occasional  vague  generalised  sensations  such  as 
hunger  or  thirst,  or  the  sense  of  well-being  following  certain 
visceral  activities,  e.g.  the  emptying  of  a  distended  bladder  or 
large  intestine,  or  the  sexual  orgasm.  In  diseased  conditions, 
however,  visceral  sensory  stimuU  may  be  so  intense  as  to  give  rise 
to  conscious  sensations.  Such  sensations  may  be  generahsed,  as 
in  the  nausea  of  gastro -intestinal  irritation  or  the  air-hunger  of 
respiratory  obstruction.  In  other  cases  the  sensations  are  localised, 
and  are  usually  referred  by  the  patient  to  the  area  of  skin  cor- 
responding to  the  nerve-root  which  conducts  the  afferent  impulse. 
Thus  we  get  the  various  "  referred  pains "  of  visceral  diseases, 
e.g.  pain  along  the  inner  border  of  the  left  arm  in  angina  pectoris, 
hyper-sesthesia  of  the  left  upper  abdomen  in  gastric  ulcer,  pain  in 
the  testicle  and  hyper-aesthesia  of  the  scrotum  in  renal  calculus, 
and  so  on.  Moreover,  certain  symptoms  in  hysterical  and  neur- 
asthenic patients  are  strongly  suggestive  of  visceral  hyper- aesthesia 
(censesthopathy),  where  normal  stimuli,  which  in  health  are  un- 
perceived,  reach  a  morbidly  sensitive  consciousness. 

Every  organ,  whether  hollow  muscular  organ,  blood-vessel,  or 
gland,  which  is  innervated  by  the  vegetative  system,  has  a  double 
innervation,  partly  derived  from  the  sympathetic  proper  and  partly 
from  the  automatic  system,  cranial  or  sacral.  This  innervation 
is  not  only  a  double  one,  but  its  two  elements  are  mutually  antago- 
nistic, hke  a  pair  of  reins.  Under  normal  conditions  these  two 
forces  are  in  equilibrium.  According  as  the  sympathetic  or  the 
autonomic  influence  predominates,  so  do  we  have  variations  in 
the  activity  of  the  particular  organ.  Thus,  for  example,  the  heart 
receives  autonomic  (inhibitory)  impulses  from  the  vagus,  and  sym- 
pathetic (accelerator)  fibres  through  the  superior  cervical  ganglion 
of  the  sympathetic.  The  intestine,  on  the  other  hand,  receives 
autonomic  (motor)  fibres  from  the  vagus  and  sympathetic  (inhibi- 
tory) impulses  through  the  splanchnic  nerve.  At  the  lower  end 
of  the  intestine  the  vagal  autonomic  fibres  are  replaced  by  those 
of  the  nervi  erigentes  derived  from  the  sacral  autonomic  system. 
The  genital  organs  receive  their  autonomic  (vaso -dilator)  fibres 
through  the  nervi  erigentes  and  their  sympathetic  (vaso-constrictor) 
fibres  from  the  hypogastric  plexus. 


356  NEEVOUS    DISEASES 

Relation  of  the  Vegetative  System  to  various  Drugs  and 
to  the  Ductless  Glands  :— 

Autonomic  fibres  and  end-organs  are  specially  stimulated 
by  cholin  bodies  and  by  pilocarpin.  They  are  paralysed  by 
alkaloids  of  the  atropin  group.  Cholin,  a  product  of  normal 
tissue-metabolism,  circulates  in  the  blood-stream  and  acts 
as  a  hormone,  exercising  its  specific  action  on  the  autonomic 
system.  Autonomic  stimulation  is  evidenced  by  some  of  the  fol- 
lowing phenomena  : — myosis,  deficient  gastro -intestinal  peristalsis, 
contraction  of  the  uterus,  ureter,  bladder,  and  bronchial  muscle, 
slowness  and  feebleness  of  the  heart,  paresis  of  the  abdominal 
blood-vessels,  pallor  of  the  skin,  increase  of  glandular  secretions 
throughout  the  body,  &c.  These  effects,  however,  are  not  produced 
all  at  one  and  the  same  time. 

Sympathetic  fibres  and  end-organs,  on  the  other  hand,  are  un- 
affected by  the  cholin  group.  They  are  not  paralysed  by  any 
agent  yet  known  to  us,  but  are  readily  stimulated  by  the  hormones 
of  chromophile  glands,  i.e.  by  adrenalin  and  its  allies.  This  re- 
action of  sympathetic  fibres  to  adrenalin  is  intensified  by  certain 
other  substances,  such  as  cocaine,  thyroid  secretion  (as  in  patients 
with  exophthalmic  goitre,  in  whom  a  few  drops  of  adrenalin,  in- 
stilled into  the  eye,  may  produce  mydriasis  markedly  in  excess  of 
the  normal),  pituitrin  (with  its  special  action  on  the  intestinal  and 
uterine  walls),  &c.  The  emotion  of  fear  is  found  to  liberate  an  excess 
of  adrenalin  into  the  blood-stream.  It  will  be  remembered  that 
the  cells  of  the  supra-renal  medulla,  constituting  the  so-called 
para-ganglion  cells,  are  derived  from  the  same  source  as  those  of 
the  sympathetic  ganglia.  The  supra-renal  gland  is  thus  partially  a 
part  of  the  nervous  system,  and  its  para-ganglion  cells  secrete  the 
adrenalin  which  maintains  the  sympathetic  cells  in  their  normal 
state  of  activity.  Morphine  has  a  special  action  in  depressing  the 
sympathetic  nuclei  situated  within  the  central  nervous  system, 
so  that  the  autonomic  system  becomes  unopposed,  and  as  a  conse- 
quence we  have  myosis,  bradycardia,  excessive  sweating,  &c. 

Vago-tonus  and  Sympathetico-tonus — Individuals  may  be 
classified  into  two  great  vegetative  types,  according  as  their  auto- 
nomic sensitiveness  prevails  over  their  sympathetic,  or  vice  versa. 
The  character  of  an  individual  may  thus  depend  largely  upon  his 
reaction  to  cholin  or  adrenalin,  or  upon  the  relative  abundance 
with  which  cholin  and  adrenalin  are  produced  in  his  organism. 


AFFECTIONS  OF  VEGETATIVE  NERVOUS  SYSTEM     357 

Thus  the  autonomic  or  vago-tonic  type  of  person  is  reserved  and 
"  cold-blooded,"  with  slow  pulse,  contracted  pupils,  deep-set  eyes, 
and  cool,  pale  skin,  which  sweats  easily  and  sometiiTies  in  patches  ; 
whilst  the  sympathetico-tonic  type  is  lively  and  excitable,  with 
rapid  heart,  bright  eyes,  dilated  pupils,  rosy  colour,  and  a  warm, 
dry  skin.  Vago-tonic  individuals  often  show  other  evidences  of 
excessive  vagal  activity  in  the  form  of  gastric  hyper-acidity,  brady- 
cardia, mild  respiratory  arrhythmia,  and  sluggish  bowel  action, 
approaching  to  spastic  constipation.  They  are  also  hyper- sensitive 
to  vagal  stimulation  by  vago-tropic  substances  such  as  pilocarpin 
(evidenced  by  bradycardia,  ready  sweating,  saUvation,  nausea  or 
vomiting,  intestinal  peristalsis,  &c.,  produced  by  this  drug),  and  to 
vagal  depression  by  atropin  (shown  by  acceleration  of  the  pulse  and 
slowing  of  intestinal  movements).  The  symptoms  of  sea- sickness 
are  often  vago-tonic  in  origin,  and  may  then  be  obviated  by  atropin 
hypodermically.  Vago-tonia  may  be  a  family  stigma.  It  may  be 
generalised  all  through  the  body,  or  we  ma}^  find  a  locahsed  vago- 
tonia, limited  to  the  cranial,  the  cervical,  or  the  sacral  division  of 
the  autonomic  system.  Vago-tonic  women  sometimes  have  a  mascu- 
line distribution  of  the  pubic  hair,  which,  instead  of  being  bounded 
above  by  a  horizontal  line,  extends  upwards  along  the  linea  alba 
towards  the  umbilicus.  These  women  have  small  mammary  glands, 
and  often  a  ring  of  hair  around  the  nipples. 

Sympathetico-tonic  individuals  are  specially  sensitive  to  adre- 
nalin, which  exaggerates  all  their  characteristics. 

The  cervical  part  of  the  sympathetic  chain  has  very  special  "  oculo- 
piipiUary  "  fibres,  which  are  of  considerable  clinical  importance.  These 
supply  the  dilator  pupillse,  the  non-striated  part  of  the  levator  palpebrse 
superioris  and  the  orbital  muscle  of  Miiller — a  small  bundle  of  non- 
striated  muscle  which  lies  behind  the  globe  of  the  eye  and  bridges 
across  the  spheno-maxillary  fossa  at  the  back  of  the  orbit.  The  cervical 
sympathetic  also  supplies  secretory  fibres  to  the  submaxillary  gland, 
and,  like  the  sympathetic  elsewhere,  it  supplies  to  the  cutaneous  blood- 
vessels, also  (through  the  hypoglossal  nerve)  to  the  vessels  of  the 
tongue,  and,  lastly,  fibres  to  the  sweat-glands  of  the  head  and  neck. 

The  pupil-dilating  fibres  have  a  peculiar  course,  which  it  is  im- 
portant to  remember  (see  Fig.  18-3).  Arising  from  the  cortical  centre 
in  the  frontal  lobe,  traversing  the  brain-stem  to  the  pupil-dilating 
centre  in  the  medulla,  they  descend  in  the  lateral  column  of  the  spinal 
cord  to  the  cilio-spinal  centre  in  the  lower  cervical  region.  They 
emerge  from  the  cord  through  the  anterior  roots  of  the  first  and  second 
thoracic  segments;  and  enter  the  inferior  cervical  ganglion  of  the 
cervical  sympathetic  by  white  rami  communicantes.     They  then  ascend 


358 


NERVOUS    DISEASES 


in  the  cervical  sympathetic  to  the  Gasserian  ganglion  and  pass  thence 
to  the  orbit  (along  the  ophthalmic  division  of  the  fifth  cranial  nerve), 
and  via  the  long  ciliary  nerves  to  the  pupil.  They  do  not  traverse  the 
ciliary  ganglion  (see  Fig.  61,  p.  138). 

It  is  evident  that  ocular  and  other  symptoms  may  be  produced 
not  only  by  lesions  of  the  ascending  fibres  of  the  cervical  sympa- 


To  noih-striatedb  part  of/ 
Iiev.PaZp.Svf). 


MEDUZLA] 


Upper  Zidj. 


alio  -spinal  CenJtre- 


^.^^DHodborFixpiXLoji 
Long  CUixxry  Nerves. 

Gasserixinj  GangUon/. 

^Muscle  of  MiiULer 
{ncrv-strLobbeob). 

To  Hyp  oglossaJLNerve. 
M     _,^^,^S%veajbFibres. 
1  ^^^^^"^Vaso-motor  & 
/y^  Vcuso- dilator  Fibres. 

Middle  CerviccCL  GanglioTv. 


^  Inferior  Cervical  GoLnglion 


Fig.  183. — Diagram  of  course  of  oculo-pupillary  fibres  of  cervical 
sympathetic. 

thetic,  but  also  by  lesions  within  the  cord,  affecting  the  fibres  in 
their  downward  course  from  the  medulla  (this  being  remarkably 
frequent  in  syringobulbia  and  in  unilateral  lesions  of  the  medulla), 
or  by  lesions  of  the  first  two  thoracic  nerves  or  of  their  anterior 
roots,  or  even  by  lesions  of  the  ophthalmic  division  of  the  fifth 
cranial  nerve,  though  this  last  is  rare. 

The  signs  of  paralysis  of  the  cervical  sympathetic  are  very  char- 


AFFECTIONS  OF  VEGETATIVE  NERVOUS  SYSTEM     359 

acteristic.  Fig.  184  shows  a  woman  who  was  sent  to  hospital  with 
the  history  that  six  years  previously  she  had  some  tuberculous 
glands  removed  from  the  right  side  of  her  neck.  When  she 
recovered  from  the  anaesthetic,  she  learned  that  the  jugular  vein 
had  been  injured  during  the  operation.  But  other  structures  had 
also  been  injured,  and  amongst  them  was  the  cervical  sympathetic 
(which  lies  behind  the  carotid  sheath),  because  afterwards  she 
noticed  that   the    right   eyelid   drooped   a   little,   that   the   right 


Fig.  184. — Paralysis  of  cervical  sympathetic  on  the  right  side.  The 
black  line  encloses  an  area  of  anaesthesia,  due  to  division  of 
cutaneous  nerves. 

side  of  the  face  flushed  less  than  the  left,  and  that  when  she 
chewed,  a  small  patch  of  excessive  perspiration  appeared  below 
the  right  eye.  We  observe  from  the  photograph  that  the  right 
pupil  is  smaller  than  the  left,  from  paralysis  of  the  dilator 
pupillse.  Moreover,  the  affected  pupil  does  not  dilate  when 
shaded,  yet  it  contracts  briskly  to  hght  and  on  convergence, 
since  the  third  cranial  nerve,  which  through  the  ciliary  ganglion 
innervates  the  sphincter  pupillae,  is  unaffected.  Further,  we 
notice  that  the  upper  lid  droops,  making  the  palpebral  fissure 
narrower  than  on  the  healthy  side.      This  is  due  to  paralysis  of 


360  NERVOUS   DISEASES 

the  non-striated  part  (tarsalis  superior)  of  the  levator  palpebrse, 
which  is  inserted  into  the  upper  edge  of  the  tarsal  cartilage.  The 
voluntary,  striated  fibres  of  the  levator,  inserted  into  the  skin  of  the 
upper  hd  and  supplied  by  the  oculo- motor  nerve,  are  unaffected, 
and  the  patient  is  therefore  able  to  elevate  the  hd  voluntarily 
to  its  full  extent.  This,  therefore,  is  not  a  true  ptosis,  but  a 
"  pseudo-ptosis." 

We  also  notice  that  the  right  eye  has  sunk  into  the  orbit,  owing 
to  paralysis  of  the  non-striated  orbitalis  muscle  of  Miiller,  which 
normally  keeps  the  globe  pressed  forwards.  This  "  enophthalmos  " 
narrows  the  palpebral  fissure  still  more.  The  difference  in  antero- 
posterior projection  between  the  two  eyes  is  seen  best  if  we  make 
the  patient  lie  down :  we  then  stand  behind  and  look  down  at 
the  forehead  and  eyeballs  from  above. 

On  palpating  the  two  globes,  we  find  that  the  intra-ocular 
tension  is  diminished  on  the  affected  side. 

Such  are  the  "  oculo-pupillary  "  symptoms  of  cervical  sympa- 
thetic paralysis.  There  are,  however,  one  or  two  additional  points. 
When  the  cervical  sympathetic  is  paralysed,  it  no  longer  responds 
to  stimulation.  There  are  two  clinical  ways  of  stimulating  it.  One 
is  by  pinching  or  pricking  the  side  of  the  neck,  when  we  produce  a 
dilatation  of  the  pupil  on  the  same  side ;  this  "  cilio-spinal  reflex  " 
is  abohshed  in  cervical  sympathetic  palsy.  Another  method  of 
stimulating  the  cervical  sympathetic  is  to  drop  into  the  conjunctiva 
a  few  minims  of  a  5  to  10  per  cent,  solution  of  cocaine.  The  result 
is  that  the  pupil  dilates,  the  upper  lid  retracts,  and  the  eyeball 
is  pushed  slightly  forwards.  All  these  phenomena  were  absent  in  the 
patient  just  referred  to.  She  also  told  us  that  when  her  face  flushes, 
it  does  so  only  on  the  healthy  side.  Moreover,  her  face  on  the 
affected  side  no  longer  sweats  except  in  one  httle  patch  below  the 
orbit,  where  it  sometimes  sweats  spontaneously  when  she  chews. 
To  verify  this  point  we  made  her  sweat  profusely  by  means  of 
pilocarpin,  and  found  that  the  right  side  of  the  face  remained  dry, 
except  in  a  small  area  below  the  inner  canthus  of  the  eye.  This 
survival  of  a  little  oasis  of  sweating  on  the  dry  side  might  perhaps 
mean  that  a  small  twig  of  the  sympathetic  had  escaped  injury, 
or  more  probably  that  sweat  fibres  to  that  part  of  the  face  are 
supplied  through  cranial  autonomic  fibres. 

So  much  lor  lesions  of  the  cervical  sympathetic  chain  itself.  But 
the  oculo-pupillary  and  other  fibres  may  also  be  damaged  at  some 


AFFECTIONS  OF  VEGETATIVE  NERVOUS  SYSTEM     361 

point  between  the  spinal  cord  and  the  inferior  cervical  gangUon. 
Fig.  185  represents  a  boy  of  seventeen  who  had  felt  a  tingling  sensa- 
tion down  his  left  arm  for  several  months.  A  few  weeks  before 
he  came  under  observation,  he  noticed  that  a  swelling  had 
appeared  in  the  lower  part  of  the  neck  on  the  same  side.  At  a 
glance  we  see  that  the  cervical  sympathetic  is  affected.  There 
are  pseudo-ptosis,  myosis,  and  enophthalmos.  The  left  cheek 
is    a    little  fuller   than    the    right.      The    cilio-spinal    reflex    was 


Fig.  185. — Paial}>itf  of  the  left  cervical  sympathetic  from  a  tumour 
at  the  root  of  the  neck. 


absent  on  the  left  side.  On  examining  the  root  of  the  neck, 
we  found  that  the  left  clavicle  was  bulged  forwards  at  its  inner 
end,  the  supra-clavicular  fossa  being  filled  up.  Further,  there 
was  percussion-dulness  all  over  the  apex  of  the  left  lung,  with 
diminution  of  breath  sounds  and  of  vocal  resonance.  There  was 
also  a  strip  of  diminished  sensation  to  touch  and  pain  along  the 
inner  side  of  the  left  upper  limb,  reaching  to  the  wrist  and  corre- 
sponding to  the  cutaneous  areas  of  the  first  and  second  thoracic  roots. 
Moreover,  there  was  shght  wasting  of  the  hypothenar  muscles  of 
the  left  hand,  supplied  by  the  first  thoracic  root.  The  skin  of 
the  left  hand  was  dry,  whilst  that  of  the  right  was  moist,  and  the 


362 


NERVOUS   DISEASES 


patient  himself  noticed  that  in  hot  weather  only  the  right  side  of 
his  face  sweated.  On  comparing  corresponding  arteries  of  both  sides 
we  found  that  the  pulse  in  the  left  upper  limb  was  smaller  than  in 
the  right.  All  this  pointed  to  the  presence  of  a  sohd  mass  behind 
the  left  clavicle,  compressing  the  subclavian  artery,  affecting  the 
first  and  second  thoracic  nerves,  including  not  only  their  sensory  and 
motor  fibres  but  also  the  cervical  sympathetic  fibres.  This  diagnosis 
was  confirmed  by  radiography,  which  showed  very  clearly  (Fig.  186) 
a  tumour  at  the  apex  of  the  left  lung.     This  tumour  grew  rapidly, 


ii 

Fig.  186. — Kadiogram,  showing  tumour  at  apex  of  left  lung, 
in  patient  represented  in  Fig.  185. 


compressed  the   subclavian  vein,    producing   oedema   of  the   left 
upper  limb,  and  within  six  months  the  patient  died. 

Fig.  187  is  that  of  a  seaman  on  an  Atlantic  liner  who  was 
thrown  against  an  iron  rail  by  a  heavy  sea,  rupturing  the  whole 
of  the  brachial  plexus  on  the  right  side.  He  was  unconscious 
for  a  number  of  days,  and  during  this  period  he  was  trephined 
over  the  left  Rolandic  area  on  the  supposition  that  the  paralysis 
of  the  arm  was  of  cerebral  origin.  In  addition  to  complete  motor 
and  sensory  paralysis  of  the  upper  limb,  obviously  of  lower  motor 
neurone  type,  resulting  from  the  brachial  plexus  palsy,  he  showed 
very  beautifully  the  oculo-pupillary  signs  of  cervical  sympathetic 
paralysis  on  the  right  side — enophthalmos,  myosis  and  pseudo- 
ptosis (see  Fig.  188).  In  this  patient,  however,  the  pupil  still 
dilated  to   cocaine,  probably  because   some   pupil-dilating   fibres, 


AFFECTIONS  OF  VEGETATIVE  NERVOUS  SYSTEM     363 

entering  the  cervical  sympathetic  from  the  second  thoracic  root, 
had  escaped  injiuy. 

Figs.  189  and  189a  are  those  of  a  soldier  who  came  under  my 
observation  during  the  South  African  war  in  1901.  He  had  been 
wounded  in  the  neck  by  a  Mauser  bullet.  At  the  time  of  his 
injury  he  was  lying  on  his  face,  firing  at  the  enemy.  The  bullet 
entered  his  neck  an  inch  and  a  half  below  the  left  mastoid  process, 


i        i 


Fig.  187. — Rupture  of  brachial  plexus  on  right  side.     Total  anaesthesia 
of  right  upper  limb  below  black  line. 

crossed  the  middle  line  in  front  of  the  vertebral  column,  and  came 
out  through  the  seventh  right  interspace  in  the  posterior  axillary 
line,  lodging  in  his  bandoher.  He  immediately  felt  a  sensation 
"  hke  an  electric  shock  "  all  over  his  body,  but  especially  in  the 
right  upper  extremity,  which  became  at  once  totally  paralysed. 
He  had  haemoptysis  owing  to  the  perforation  of  the  lung,  and 
for  a  few  days  some  difficulty  of  swallowing,  probably  due  to  injury 
of  the  oesophagus.  In  about  three  weeks  the  hsemoptysis  gradually 
ceased,  and  the  right  upper  limb  recovered  power,  so  that  when 


364  NERVOUS    DISEASES 

I  first  saw  him,  two  and  a  lialf  montlis  after  tlie  injury,  he  was 
able  to  move  it  freely  at  all  joints.  Ever  since  the  accident  he 
had  noticed  that  he  did  not  sweat  on  the  right  side  of  the  face 
and  neck,  nor  in  the  right  upper  hmb. 

The  photographs  show  that  the  patient  has  an  area  of  shght 
analgesia  (bounded  by  the  thick  black  line)  along  the  inner  border 
of  the  right  upper  Hmb,  corresponding  to  the  areas  supphed  by 
the  eighth  cervical,  first  thoracic,  and  second  thoracic  nerve-roots. 
He  also  has  slight  weakness  of  the  small  muscles  of  the  thumb. 


Fig.  188. — Paralysis  of  right  cervical  sympathetic  from  rupture  of 
brachial  plexus. 

innervated  by  the  first  thoracic  root.  We  also  observe  that  the 
right  cervical  sympathetic  is  paralysed,  so  that  he  has  contraction 
of  the  pupil,  enophthalmos,  and  pseudo-ptosis  on  that  side. 

But  there  is  a  point  of  special  interest  in  this  patient's  photo- 
graphs. They  demonstrate  a  point  which,  so  far  as  I  know,  had 
not  previously  been  mapped  out  in  the  human  subject,  viz.,  the 
extent  of  skin  supplied  with  sweat-fibres  by  the  cervical  sympa- 
thetic. In  the  tropical  heat  to  which  we  were  exposed,  this 
patient  sweated  profusely,  except  in  an  area  on  the  right  side 
of  the  head,  neck,  upper  limb,  and  upper  part  of  the  trunk.  That 
area  remained  dry,  and  the  boundary  between  sweating  and  non- 
sweating  skin  was  sharp  and  distinct.     In  order  to  show  this  in  a 


AFFECTIONS  OF  VEGETATIVE  NERVOUS  SYSTEM     365 


photograph,  the  happy  thought  occurred  to  blow  powdered  charcoal 
on  the  skin.  This  stuck  on  the  sweating  side,  and  was  blown  off  on 
the  dry  side.  We  were  then  able  to  photograph  the  non-sweating 
area,  to  which  the  cervical  sympathetic  should  have  been  dis- 
tributed. As  may  be  seen  from  the  pictures  (Figs.  189  to  190),  the 
boundary  of  this  area,  marked  by  crosses,  runs  down  the  middle 
line   of  the   head  and  neck,   and    turns    horizontally    across   the 


Fig.  1S9a. 


Figs.  189  and  189a.— Paralysis  of- the  right  cervical  sympathetic,  from  a 
bullet  wound  of  the  lower  roots  of  the  brachial  plexus.  The  area 
of  the  right  upper  limb  within  the  black  line  is  anaesthetic.  The 
crosses  on  the  trunk  indicate  the  boundary  of  an  area  of  anidrosis. 

chest  at  the  level  of  the  third  rib  in  front  and  of  the  spine  of 
the  scapula  behind,  including  the  whole  of  the  upper  limb. 

Before  leaving  the  subject  of  cervical  sympathetic  palsy,  it 
should  be  mentioned  that  excision  of  the  cervical  sympathetic 
has  been  employed  therapeutically  in  certain  diseases.  Thus 
in  cases  of  glaucoma,  ophthalmic  surgeons  have  recommended 
this  operation  to  diminish  the  intra-ocular  tension,  and  a  certain 
amount  of  benefit  has  resulted.  Bilateral  excision  of  the 
cervical  sympathetic  has   also  been  tried  for  the  rehef  of    epi- 


366  NERVOUS    DISEASES 

lepsy,  in  the  hope  of  paralysing  the  cerebral  vasomotor  nerves 
and  thereby  rendering  the  brain  hypersemic,  especially  in  cases 
in  which  fits  were  ushered  in  by  blanching  of  the  face.  But  the 
results  recorded  have  not  been  sufficiently  good  to  warrant  us  in 
recommending  this  procedure. 

Let  us  now  consider  briefly  the  reverse  condition,  viz.,  irrita- 
tion or  stimulation  of  the  cervical  sympathetic.  The  signs  are 
exactly  the  opposite  of  those  produced  by  paralysis.     We  there- 


FiG.  190. — Paralysis  of  the  right  cervical  sympathetic,  showing 
oculo-pupillary  phenomena  and  area  of  anidrosis. 

fore  have  dilatation  of  the  pupil,  exophthalmos  or  forward  projection 
of  the  eyeball,  widening  of  the  palpebral  aperture  (Stellwag's  sign), 
and  delayed  descent  of  the  upper  lid  when  the  patient  looks 
downwards  (von  Graefe's  sign).  All  these  phenomena  can  be  pro- 
duced, to  a  certain  degree,  by  dropping  into  a  healthy  eye  a 
solution  of  cocaine,  which  stimulates  the  cervical  sympathetic. 

Fig.  191  is  that  of  a  man  who  had  lymphadenomatous  en- 
largement of  the  lymphatic  glands.  During  his  stay  in  hospital, 
we  noticed  that  quite  rapidly,  within  a  day  or  two,  he  developed 
on  the  right  side  exophthalmos,  widening  of^  the  palpebral  fissure, 
and  some  dilatation  of  the  pupil.      There  was  also  in  hospital  at 


AFFECTIONS  OF  VEGETATIVE  NERVOUS  SYSTEM     367 

the  same  time  a  soldier  who  had  similar  signs  in  one  eye  due  to 
an  aneurism  at  the  root  of  the  neck,  pressing  on  and  irritating  the 
cervical  sympathetic.  If  such  pressure  continues,  the  signs  of 
stimulation  may  pass  oE  and  be  replaced  by  those  of  paralysis. 
Our  lymph  adenomatous  patient,  however,  died  nine  weeks  after 
the  appearance  of  stimulation  phenomena,  without  any  change 
in  the  direction  of  paralysis. 

Certain    cases    of     apical     phthisis     and     apical     pneumonia 


Fig.  191. — Stimulation  of  the  right  cervical  sympathetic. 

are  accompanied  by  inequality  of  the  pupils,  probably  due 
to  irritation  of  the  cervical  sympathetic  by  changes  in  the 
pleura. 

Many  of  the  signs  of  exophthalmic  goitre  are  sympathetico- 
tonic,  resulting  from  excessive  or  perverted  thyroid  secretion. 
Figs.  192  and  192a  are  from  a  case  of  exophthalmic  goitre  in  which 
the  symptoms  are  preponderatingly  right-sided.  The  tachycardia 
of  this  disease  is  probably  due  to  stimulation  of  sympathetic  cardio- 
accelerator  fibres.  The  thyroid  enlargement  may  be  in  part  the 
result  of  vasomotor  paralysis  of  the  cervical  vessels,  including 
those  of  the  thyroid  gland  itself.     The  excess  of  lymphocytes  and 


368 


NERVOUS    DISEASES 


of  eosinophiles  in  tlie  blood,  together  with  the  diminution  of  poly- 
morphs, is  probably  also  a  result  of  the  disordered  thyroid  secretion, 
which  induces  these  blood-changes  indirectly  by  producing  hyper- 
plasia and  hyper-activity  of  the  thymus  and  of  the  lymphatic 
glands. 

But  though  affections  of  the  cervical  sympathetic  are  the  most 
readily   recognised,    we    must    not   forget    that   the    thoracic   and 


I'IG.  102. 


Fig.  192  .a 


Exophthalmic  goitre,  the  ocular  symptoms  being  more  marked  on  the  right 
side.  Fig.  192a  shows  von  Graefe's  sign  in  the  right  eye  on  looking 
downwards. 

abdominal  portions  of  the  sympathetic  may  also  be  diseased, 
although  the  symptoms  thereby  produced,  being  mainly  visceral, 
are  less  easy  of  diagnosis.  Thus  some  cases  of  angina  pectoris 
may  be  the  result  of  irritation  of  aortic  fibres  from  the  cardiac 
plexus,  while  the  peculiar  reflex  vaso-constriction  of  the  pulmonary 
vessels,  with  transient  dilatation  and  irregularity  of  the  right 
heart,  met  with  in  certain  gastric  and  hepatic  disorders,  has  been 
regarded  as  an  affection  of  the  thoracic  part  of  the  sympathetic. 
Affections  of  the  abdominal  vegetative  system  produce  still  more 
striking    clinical    phenomena.     An    important    group    of    nervous 


AFFECTIONS  OF  VEGETATIVE  NERVOUS  SYSTEM     369 

dyspepsias  is  associated  with  excessive  vago-tonus,  notably  cases 
with  hyper-acidity,  pyloric  spasm,  and  excessive  gastric  contraction 
evidenced  by  loud  peristaltic  rumbling  noises.  In  such  cases  (as 
also  in  lead-poisoning)  treatment  by  atropin  often  has  a  markedly 
beneficial  effect.  The  rare  condition  known  as  acute  dilatation 
of  the  stomach,  and  many  of  the  symptoms  of  acute  perito- 
nitis, such  as  the  intestinal  paralysis,  meteorism,  small  pulse,  and 
general  collapse,  may  be  the  result  of  acute  paralysis  of  the  solar 
plexus — the  "  abdominal  brain  "  ;  while  irritation  of  the  solar 
plexus,  and  especially  of  its  autonomic  fibres,  is  exemphfied  in 
cases  of  lead  colic,  with  its  pain,  constipation,  and  increased  arterial 
tension.  The  various  visceral  "  crises  "  of  tabes — gastric,  intes- 
tinal, renal,  &c. — may  also  be  due  to  irritative  changes  in  various 
parts  of  the  autonomic  system.  To  the  same  cause  also  may  be 
attributed  the  intestinal  symptoms  of  exophthalmic  goitre,  con- 
sisting not  in  ordinary  diarrhoea  with  loose  motions,  but  rather  in 
an  abnormal  frequency  of  defaecation.  Spastic  constipation,  with 
its  hard  dry  stools,  and  also  muco-membranous  cohtis,  with  its 
paroxysms  of  increased  peristalsis,  accompanied  by  an  excessive 
secretion  of  intestinal  mucus,  are  probably  both  evidences  of  vago- 
tonus,  and  are  often  relieved  by  atropin.  The  apparent  contra- 
diction in  ascribing  constipation  and  diarrhoea  to  the  same  cause  is 
explicable  by  the  fact  that  in  the  one  condition  the  circular  muscle- 
fibres  of  the  intestine  are  affected,  producing  constipation,  whilst 
in  the  other  the  longitudinal  fibres  are  affected,  permitting  diarrhoea. 
To  solar  or  splanchnic  disease  may  also,  perhaps,  be  attributed 
such  affections  as  orthostatic  albuminuria  and  certain  forms  of 
glycosuria,  and  diabetes  insipidus. 

In  addition  to  visceral  disorders,  disease  of  the  abdominal  sym- 
pathetic is  also  associated  with  certain  pigmentary  changes  in  the 
skin.  Of  these,  the  most  striking  examples  are  furnished  by  the 
cutaneous  pigmentation  which  is  occasionally  present  in  exoph- 
thalmic goitre  and,  still  more,  by  Addison's  disease,  with  its  char- 
acteristic bronzing  of  the  skin,  its  asthenia,  its  extraordinarily  low 
blood-pressure,  and  its  paroxysmal  diarrhoea.  The  symptoms  of 
Addison's  disease  are  probably  the  result  of  two  factors — irritation 
of  the  abdominal  sympathetic  and  inadequacy  of  suprarenal 
secretion,  the  proportional  role  played  by  each  of  these  varying  in 
difierent  cases. 

Anglo-Neuroses. — These  comprise  a  group  of  diseases  which 

2  A 


370  NERVOUS    DISEASES 

appear  to  depend  on  disorders  of  the  vegetative  fibres  which  regu- 
late the  heart  and  blood-vessels. 

Amongst  the  commonest  of  these  affections  are  the  curious 
paroxysms  to  which  Growers  has  given  the  name  of  vaso-vagal 
attacks.  These  appear  to  be  due  to  disorder  of  that  part  of  the 
cranial  autonomic  system  which  comprises  the  vagal  distribution 
to  the  heart,  lungs,  and  other  organs.  The  attack  generally  begins 
with  an  epigastric  aura,  quickly  followed  by  violent,  irregular,  and 
rapid  beating  of  the  heart,  together  with  a  sense  of  suffocative 
dyspnoea  and  sometimes  a  feeling  of  impending  death.  Mean- 
while the  limbs  become  very  cold,  followed  either  by  burning  flushes 
or  clammy  sweat,  and  a  distressing  tension  of  the  muscles.  The 
paroxysms,  varying  in  duration  from  a  few  minutes  to  several 
hours,  recur  at  irregular  intervals.  They  are  specially  common  in 
women  at  the  menopause.  They  can  often  be  alleviated  by  small 
doses  of  nitro-glycerine. 

A  considerable  amount  of  evidence  ^  points  to  the  conclusion 
that  the  paroxysmal  unconsciousness  of  epilepsy  is  associated 
with  sudden  cerebral  ansemia  and  that  the  tonic  stage  of  a  major 
epileptic  fit  is  accompanied  by  cortical  anaemia,  whilst  the  clonic 
stage  is  associated  with  return  of  arterial  circulation.  It  is  un- 
certain what  proportion  of  these  phenomena  is  due  to  sudden 
stoppage  of  the  heart  (we  may  sometimes  feel  the  patient's  pulse 
stop  at  the  onset  of  a  fit)  and  how  much  to  vasomotor  spasm  of 
cortical  vessels. 

The  paroxysmal  expiratory  dyspnoea  of  asthma,  with  the  slow 
and  laboured  breathing,  is  doubtless  due  to  excessive  vago-tonus. 
The  phenomena  may  either  be  the  immediate  result  of  a  sudden  vas- 
cular engorgement  of  the  bronchial  mucous  membrane,  or  may  be 
produced,  according  to  another  view,  by  spasm  of  the  non-striated 
bronchial  muscles,  innei'vated  by  autonomic  fibres  in  the  vagus. 
Asthma  is  often  reheved  by  atropin  or  by  adrenahn,  both  of  which 
drugs  depress  the  vagus.  In  any  case,  the  paroxysmal  nature  of 
the  affection,  its  apparent  toxic  origin  in  some  cases,  its  connection 
in  other  cases  with  nasal  or  other  reflex  sources  of  irritation,  its 
frequent  association  with  the  gouty  diathesis — all  indicate  a 
functional  and  not  an  organic  lesion  of  the  autonomic  nervous 
mechanism. 

Most  angio-neuroses,  however,  affect  the  blood-vessels  of  the 

1  A.  E.  Russell,  Lancet,  If  0:>,  April  3,  10,  and  17. 


AFFECTIONS  OF  VEGETATIVE  NERVOUS  SYSTEM     371 

more  superficial  parts  of  the  body,  such  as  those  of  the  skin  or  of 
the  muscles.  Amongst  the  cutaneous  angio-neuroses,  perhaps  the 
commonest  is  the  syndrome  known  as  angio-spastic  gangrene,  or 
Raynaud's  disease.  The  mildest  degree  of  this  is  local  jjallor  ("  local 
syncope  "  or  "  dead  finger  "),  where  the  affected  parts,  usually  the 
fingers,  less  frequently  the  toes,  the  edges  of  the  ears,  or  the  tip  of 
the  nose,  suddenly  become  cold  to  the  touch  and  of  a  waxy 
white  colour.  Together  with  this,  the  patient  feels  a  tingling 
or  other  peculiar  sensation  (acro-parsesthesia).  Actual  blunting  of 
sensation  to  touch  may  be  present.  One  or  both  hands  may  be 
affected,  sometimes  identical  fingers  in  both  hands  ;  the  thumb 
is  less  often  affected  than  the  other  digits.  The  attacks  last  from 
a  few  minutes  to  several  hours  and  are  commonest  in  winter. 
They  are  often  brought  on  by  washing  the  hands  in  cold  water,  or 
by  fine  digital  movements  such  as  sewing  or  piano-playing.  As  the 
attack  passes  off,  the  patient  feels  a  sensation  of  tingling  or  even 
of  pain.  A  more  severe  variety  is  that  of  local  asphyxia  or  cyanosis, 
in  which  the  affected  digits  suddenly  become  discoloured,  varying 
in  tint  from  a  dusky  blue  or  slate  colour  to  an  intense  purplish- 
black.  Pressure  on  the  discoloured  area  causes  a  white  mark  which 
persists  for  several  seconds,  before  the  Hvidity  slowly  reappears. 
The  pain  is  usually  more  intense  than  in  local  syncope.  As 
the  attack  passes  off,  the  affected  part  often  sweats  freely.  But 
the  most  severe  variety  of  Raynaud's  disease  is  symmetrical 
gangrene,  which  is  usually  preceded  by  local  asphyxia  and  some- 
times by  local  syncope.  As  a  rule,  the  gangrenous  process  is 
confined  to  a  small  part  of  the  cyanosed  area.  In  its  mildest  form 
the  necrosis  is  Limited  to  the  epitheHum,  so  that  only  desquamation 
results ;  more  often  a  small  bhster  forms,  with  blood-stained 
contents.  This  bursts,  leaving  an  ulcer  which  subsequently 
cicatrises.  The  nails  may  be  lost  and  subsequently  reproduced. 
Or  the  necrosis  may  extend  deep  into  the  tissues,  forming  a  dark 
slough.  Whole  phalanges  may  undergo  dry  mummification  and 
be  cast  off,  leaving  a  conical  stump.  The  bones  as  a  rule  escape 
necrosis.  Pain  is  usually  severe  during  the  initial  cyanosis.  The 
symptoms  of  Raynaud's  disease  are  due  to  local  spasm  of 
the  vessels,  their  sudden  onset  and  disappearance  being 
incompatible  with  any  other  hypothesis.  The  coexistent  sensory 
symptoms  are  probably  due  to  imperfect  blood-supply.  A 
paroxysm  of  local  syncope   or   cyanosis  can  usually  be  relieved, 


372  NERVOUS    DISEASES 

as  Gushing  has  pointed  out,  by  applying  a  tight  flat  rubber 
tourniquet  around  the  Hmb  above,  so  as  to  occlude  all  the  vessels, 
both  arteiies  and  veins,  and  leaving  it  on  for  several  minutes. 
When  the  tourniquet  is  taken  off,  there  is  a  temporary  vaso- 
motor paralysis,  the  whole  limb  flushes  to  the  finger-tips,  and  a 
wave  of  redness  wipes  out  the  local  pallor  or  cyanosis.  In  rare 
cases  paroxysmal  impairment  of  vision  has  been  noted,  and  during 
such  attacks  the  retinal  arteries  on  ophthalmoscopic  examination 
have  been  seen  to  be  spasmodically  contracted.  In  paroxysmal 
haemoglobinuria,  Raynaud's  syndrome  is  constantly  present,  to  a 
greater  or  less  degree. 

In  striking  contrast  with  Raynaud's  disease  is  the  condition 
known  as  erythromelalgia  (see  Plate  III.),  which  usually  attacks  one 
or  other  foot.  There  is  pain  of  a  burning  or  stabbing  character, 
often  of  excruciating  severity,  occurring  in  paroxysms  lasting 
from  a  few  minutes  to  several  hours.  This  pain  is  always  aggra- 
vated by  dependent  posture  of  the  Hmb,  by  voluntary  movement, 
or  by  warmth,  whereas  it  is  diminished  by  a  horizontal  or  elevated 
posture,  by  rest,  and  by  cold  applications.  The  earHest  attacks 
consist  simply  of  pain.  As  the  disease  progresses,  however,  redness 
and  swelling  of  the  foot  are  superadded ;  more  rarely,  redness 
precedes  pain.  The  redness  is  of  a  bright  tint,  often  confined, 
for  instance,  to  the  ball  of  the  big  toe  or  to  small  areas  of  the  sole 
or  edge  of  the  foot.  Sometimes  it  is  diffused  over  the  foot.  The 
redness  increases  in  intensity,  and  if  the  limb  be  allowed  to  hang 
down,  the  "  vascular  storm "  continues,  with  bounding  arteries, 
local  rise  of  temperature,  and  intense  cutaneous  hypersesthesia. 
As  the  attack  subsides  the  redness  is  replaced  by  cyanosis.  In  one 
case  which  I  observed,  desquamation  of  the  affected  area  occurred 
after  each  paroxysm. 

But  there  are  other  cases  in  which  the  vasomotor  symptoms 
are  intermediate  in  type  between  the  two  extremes  of  Raynaud's 
disease  and  erythromelalgia.  These  two  diseases  may  coexist,  or 
may  succeed  each  other  in  the  same  patient.  Erythromelalgia  is 
sometimes  one  of  the  earhest  signs  of  organic  cord  disease,  such 
as  disseminated  sclerosis,  and  this  points  to  its  origin  from  an 
affection  of  the  spinal  vasomotor  centres,  probably  in  the  "  inter- 
medio-lateral "  group  of  smaller  nerve-cells  (nucleus  sympatheticus 
lateralis)  between  the  anterior  and  posterior  horns,  to  which  Bruce  ^ 

1   Trans.  Roy.  Soc.  of  Edin.,  1906,  vol.  xlv.  part  i.  p.  105. 


PLATE   III. 

Case  of  Erythromelalgia  in  a  man  aged  52.  The  condition  affected 
both  lower  limbs. 

The  upper  drawing  shows  the  appearance  of  one  foot  during  a 
paroxysm  when  the  lower  limb  is  supported  in  a  horizontal  position. 
The  sole  of  the  foot  is  of  a  bright  pink  colour,  this  colour  also  extending 
on  to  the  dorsum  of  the  terminal  phalanx  of  each  toe. 

The  lower  drawing  shows  the  effect  of  allowing  one  foot  to  hang 
dependent  for  a  few  minutes.  There  is  extreme  cj'auosis  extending  as 
high  as  the  ankle.  There  was  also  severe  pain,  partially  relieved  by 
reassuming  the  horizontal  posture  of  the  limb. 


To  face  page.  372. 


glMidmotdi^TSL  ?'»  aaeD 


AFFECTIONS  OF  VEGETATIVE  NERVOUS  SYSTEM     373 

directed  special  attention.  A  few  rare  cases  have  also  been  observed 
of  family  gangrene,  somewhat  resembling  Raynaud's  disease. 
Fig.  193  represents  three  brothers,  aged,  five,  four  and  three  years 
respectively,  in  all  of  whom,  one  winter,  areas  of  local  necrosis 
appeared  in  the  feet.  The  eldest  child  had  necrosis  of  the  skin  of 
both  heels,  followed  by  similar  areas  on  the  dorsum  of  the  right  foot 


Fig.  193. — Family  gangrene  in  three  brothers,  affecting  the  feet. 

F-and  on  the  fourth  left  toe.  The  second  child  had  cyanosis  and  some 
necrosis  of  the  dorsal  surfaces  of  both  feet,  whilst  the  youngest 
had  severe  necrosis  of  the  hallux,  fourth  and  fifth  toes  on  the  right 
side,  and  a  smaller  area  of  necrosis  on  the  plantar  surface  of  the 
left  hallux.  It  is  possible  that  the  paroxysms  of  family  "periodic 
paralysis  (see  p.  266)  may  be  the  result  of  a  recurring  vasomotor 
spasm  of  the  anterior  spinal  artery,  which,  as  we  have  seen,  supplies 
the  anterior  cornua  of  the  spinal  cord. 

Another  paroxysmal  disease  of  angio -neurotic  origin  is  inter- 


374  NERVOUS    DISEASES 

mittent  arterial  claudication,  the  symptoms  of  which  we  have 
already  described  (p.  263).  Here  the  arteries  not  of  the  skin  but 
of  the  deep  structures  are  in  a  state  of  temporary  spasm. 

Amongst  soldiers  defending  trenches  in  the  winter  season — as 
in  the  1914-15  campaign  in  Flanders — there  occur  numerous  cases 
of  trench-foot  or  so-called  "  frost-bite."  Very  few  of  the  cases, 
however,  are  due  to  actual  frost.  The  factors  producing  the 
condition  are  exposure  of  the  feet  to  mud  and  thawing  snow,  want 
of  exercise  of  the  leg  muscles,  together  with  prolonged  constriction 
by  tight  putties  and  by  boots  which  undergo  shrinkage  when  soaked. 
The  signs  are  primarily  vascular  in  character,  to  which  may  be 
superadded  the  sensory  phenomena  of  a  peripheral  neuritis.  The 
toes  become  cold  and  pale,  in  some  cases  cyanosed  and  in  rarer 
cases  gangrenous.  There  is  slight  impairment  of  cutaneous  sensa- 
tion in  the  toes,  with  considerable  pain  and  tingling.  (Edema 
of  the  feet  may  occur,  and  in  severe  cases,  associated  with  excoria- 
tion and  infection  of  the  skin,  this  oedema  may  extend  to  the 
knees.  As  the  circulation  begins,  under  treatment,  to  return,  the 
pain  becomes  aggravated,  and  even  after  the  circulatory  pheno- 
mena have  apparently  recovered,  this  pain  may  persist,  with 
characteristic  signs  of  peripheral  neuritis,  as  shown  by  the  combina- 
tion of  impairment  of  sensation  to  light  touches  together  with 
intense  hyperaesthesia  on  pressure,  so  that  for  weeks  the  patient 
may  be  unable  to  stand  or  walk,  owing  to  pain  in  the  soles  of  the 
feet,  especially  in  their  anterior  parts. 

Acute  angio-neurotic  oedema,  or  Quincke's  disease,  is  undoubtedly 
a  vaso-neurosis.  It  is  characterised  by  paroxysmal  attacks  of 
sharply  localised,  hard  oedema  in  the  cellular  tissue  of  various  parts 
of  the  face,  trunk  or  limbs.  After  lasting  a  few  hours  or  days,  the 
swelling,  which  is  remarkably  firm  and  does  not  readily  pit  on 
pressure,  passes  off  spontaneously.  It  may  also  attack  mucous 
membranes,  for  example,  those  of  the  respiratory  or  gastro-intestinal 
tract.  A  gastric  attack  may  cause  urgent  vomiting,  an  intes- 
tinal attack  meteorism,  cohc,  and  bloody  diarrhoea,  and  if  the 
patient  happens  to  have  an  attack  in  the  larynx,  death  may 
result  from  asphyxia.  In  the  skin,  the  parts  most  often  attacked 
are  the  lips,  cheeks  and  eyehds.  The  disease  sometimes  runs  in 
families. 

In  recent  hemiplegia  we  frequently  notice  that  the  skin  on  the 
paralysed  side  of  the  body  is  warmer  than  on  the  normal  side,  the 


AFFECTIONS  OF  VEGETATIVE  NERVOUS  SYSTEM     375 

difference  in  temperature  between  the  two  axill*  being  as  much  as 
1"  F.  or  more. 

In  chronic  hemiplegia  it  is  not  uncommon  to  find  oedema  of  the 
hand  or  foot  on  the  paralysed  side.  (Edema  of  the  legs  occurs 
in  beri-beri,  probably  from  special  degeneration  of  the  vegetative 
fibres  in  this  variety  of  peripheral  neuritis.  Permanent  coldness 
and  cyanosis  are  very  common  in  the  paralysed  Umbs  in  cases 
of  old  anterior  poliomyelitis.  Even  in  warm  weather  the  flaccid 
limb  remains  cold  and  sometimes  blue  in  the  hand  or  foot,  as  the 
case  may  be.  Such  cyanosis  differs  from  that  of  Raynaud's  group 
in  being  permanent  and  not  paroxysmal. 

Certain  varieties  of  urticaria  may  be  referable  to  affection  of 
the  nervous  system,  as  in  certain  cases  in  which  the  characteristic 
itching  wheals  appear  on  sudden  emotional  excitement.  These 
patients  appear  to  have  a  specially  low  coagulability  of  the 
blood  due  to  deficiency  of  calcium  salts  in  the  liquor  sanguinis. 
But  urticaria  is  much  more  often  toxic  in  origin.  Derniographiatn, 
on  the  other  hand  ("  factitious  urticaria  "  or  "  urticaria  scripta  "), 
is  a  reflex  cutaneous  phenomenon.  It  is  ehcited  by  stroking 
the  skin  fii-mly  with  a  smooth,  hard  object,  such  as  the  head  of 
a  pin  or  the  finger-nail.  If,  for  example,  we  draw  a  diagram 
or  write  on  the  patient's  skin  in  this  way,  a  red  area  appears 
within  a  few  seconds.  The  skin  then  becomes  elevated  into 
a  hard,  white  ridge,  which  can  not  only  be  felt  but  seen,  as  if  the 
pattern  or  writing  had  been  embossed  on  the  skin  (see  Fig.  212, 
p.  414).  This  lasts  for  many  minutes  and  passes  off  gradually. 
Unlike  true  urticaria,  dermographism  is  unaccompanied  by  itching. 
The  phenomenon  is  commonest  in  neuropathic  people,  but  is  not 
confined  to  them  ;  it  is  particularly  common  in  exophthalmic 
goitre,^  and  may  sometimes  be  found  in  apparently  healthy 
individuals.  The  strange  malady  known  as  intermittent  hydrar- 
throsis appears  to  have  an  affinity  with  giant  urticaria. 

Lastly,  we  have  to  refer  to  certain  abnormalities  of  sweating 
which  are  due  to  nervous  disorders.  We  have  already  alluded  to 
localised  anidrosis  or  absence  of  sweat  in  certain  cases  of  cervical 
sympathetic  palsy.  But  sometimes  we  meet  with  'paroxysmal 
localised  hyperidrosis  or  excessive  sweating.  Figs.  194  and  195 
show"  the  areas  of  excessive  sweating  in  two  patients.  In  one  the 
condition  was  congenital,  and  consisted  in  excessive  sweating  on 

^  Dreschfeld,  Brit.  Med.  Journal,  November  18,  1905. 


376 


NERVOUS    DISEASES 


the  left  side  of  the  scalp  and  face,  corresponding  to  the  whole  of 
the  first  division  and  part  of  the  second  division  of  the  trigeminal. 
In  the  other,  the  whole  area  of  the  trigeminal  on  the  right  side  was 
affected  and  the  condition  appeared  at  the  age  of  twenty-eight. 
In  both  these  patients,  who  were  otherwise  healthy,  the  paroxysms 
of  sweating  occurred  only  on  chewing  highly-flavoured  articles, 
such  as  onions  or  pickles.  This  condition  suggests  some  hyper- 
excitability  of  the  reflex  sweating  centre  for  the  face,  possibly 
within  the  pons.  Fig.  196  is  a  photograph  of  an  area  of  hyperi- 
drosis  on  the  left  hand  and  wrist  of  a  young  woman  of  nineteen. 
In  her,  the  paroxysms  occurred  three  or  four  times  a  day,  spon- 


FiG.  194. — Area  of  localised 
sweating  during  masti- 
cation of  pungent  sub- 
stances. From  a  man 
aged  29.  The  condition 
was  congenital. 


Fig.  195. — Area  of  localised 
sweating  during  mastica- 
tion of  pungent  substances. 
From  a  man  aged  35,  in 
whom  the  condition  ap- 
peared at  the  age  of  28. 


taneously,  chiefly  about  the  time  of  the  menstrual  period  or 
when  she  was  excited.  In  this  case  the  distribution  suggested  a 
segmental  or  root  area,  apparently  about  the  eighth  cervical  and 
first  thoracic  segments,  and  counter-irritation  over  the  lower  part 
of  the  neck,  front  and  back,  near  the  exit  of  these  roots, 
produced  rapid  amelioration  of  the  condition. 

In  certain  chronic  cases  of  hemiplegia,  we  not  infrequently 
observe  excessive  sweating  of  the  hand  and  foot  on  the  paralysed 
side.  This  is  doubtless  due  to  changes  in  the  sweating  centres  in 
the  central  nervous  system. 

Transverse  lesions  of  the  spinal  cord  may  also  be  associated 
with  abnormalities  of  sweating,  owing  to  lesion  of  the  nucleus 
sympatheticus  in  the  intermedio-lateral  column  of  the  grey  matter. 


AFFECTIONS  OF  VEGETATIVE  NERVOUS  SYSTEM     377 

This  is  conveniently  demonstrated  by  means  of  a  hypodermic 
injection  of  pilocarpin,  previously,  by  a  suitable  cradle,  protecting 
the  patient's  body  from  contact  with  the  bed-clothes.     Profuse 


m^ 


^ 


Fig.  196. — Localised  hyperidrosis  along  ulnar  border  of  forearm  and  hand. 
The  dark  area  is  due  to  powdered  charcoal  adherent  to  sweating  skin. 

sweating  is  produced  in  the  parts  above  the  level  of  the  lesion, 
whereas  the  skin  of  the  lower  limbs  and  trunk  remains  dry,  up 
to  the  level  of  the  affected  segment  of  the  spinal  cord. 


CHAPTER  XXI 

THE  NEUROSES 

The  boundary  between  organic  diseases  and  the  so-called  func- 
tional diseases  or  neuroses  is  entirely  imaginary.  The  old  defini- 
tion of  a  neurosis  as  a  nervous  disease  devoid  of  anatomical 
changes  is  inadequate.  Disease  is  inconceivable  without  some 
underlying  physical  basis.  The  lesion  need  not  be  visible  micro- 
scopically ;  it  may  be  molecular  or  bio-chemical.  In  certain 
diseases,  such  as  epilepsy  and  paralysis  agitans,  the  essential 
underlying  lesion  is  still  undiscovered,  yet  we  no  longer  class 
them  as  neuroses  in  the  strict  sense  of  the  word.  Therefore  when 
we  as  physicians  talk  of  certain  syndromes  and  call  them  neuroses, 
although  we  may  have  a  fair  general  idea  of  what  we  mean,  we 
find  it  difficult  to  express  our  conception  in  words. 

In  "  functional "  nervous  diseases  the  underlying  physical 
changes  are  slight  in  degree,  and  they  are  often  capable  of  cure. 
In  this  respect  they  difier  not  only  from  ordinary  organic  diseases 
due  to  gross  anatomical  lesions,  which  almost  always  leave  behind 
them  some  permanent  damage,  but  also  from  such  steadily  pro- 
gressive and  incurable  affections  as  paralysis  agitans.  Neverthe- 
less we  must  recognise  that  the  neuroses  are  real  diseases,  with 
positive  clinical  phenomena,  as  real  as  smallpox  or  cancer.  We 
should  never  diagnose  a  neurosis  on  negative  evidence  alone,  i.e. 
merely  from  the  absence  of  signs  of  organic  disease.  To  establish 
a  secure  diagnosis,  characteristic  positive  phenomena,  physical  and 
mental,  must  also  be  present.  A  sharp  distinction  must  be  drawn 
between  a  hysterical  or  a  neurasthenic  patient  and  a  person  who 
is  deliberately  shamming  or  malingering.  The  imitation  of  other 
diseases — neuromimesis — ^which  is  often  seen  in  hysteria  is  not  a 
voluntary  affair.  The  hysterical  or  neurasthenic  patient  usually 
has  no  knowledge  of  the  disease  which  he  or  she  may  unconsciously 
simulate.  The  various  paralyses  and  pains  from  which  hysterics 
and  neurasthenics  suffer  are  as  real  to  the  patients  as  if  they  were 
due  to  gross  organic  disease. 

378 


THE    NEUROSES  379 

The  three  chief  neuroses  proper  are  neurasthenia,  psychasthenia, 
and  hysteria.  Neurasthenia  is  an  "  exogenous "  neurosis ; 
psychasthenia  is  essentially  "  endogenous  "  ;  so  also  is  hysteria, 
although  outside  factors  may  act  as  exciting  or  precipitating 
causes.  Each  of  these  neuroses  has  fairly  distinctive  character- 
istics of  its  own,  but  in  practice  they  are  often  combined  with 
each  other  and  may  also  coexist  with  organic  diseases.  Thus  a 
hysterical  patient  may  suffer  from  neurasthenia,  or  a  psychasthenic 
patient  from  hysteria  ;  nor  is  there  anything  to  prevent  a  neuras- 
thenic or  hysterical  patient  from  having,  say,  an  attack  of  cerebral 
haemorrhage.  Moreover,  any  gross  organic  disease  may  induce 
hysterical  or  neurasthenic  phenomena  in  addition  to  the  signs  of 
organic  lesion.  In  fact  certain  forms  of  grave  organic  disease 
(especially  disseminated  sclerosis  and  some  cerebral  tumours)  may 
at  first  produce  symptoms  which  are  indistinguishable  from  those 
of  functional  disease — ^which  are,  in  fact,  functional.  In  such 
cases  the  neurologist  must  be  on  his  guard  to  detect  the  underlying 
organic  affection,  and  to  distinguish  its  symptoms  from  those  of 
the  superadded  hysteria  or  neurasthenia.  Functional  symptoms, 
then,  may  coexist  with  gross  organic  disease. 

Let  us  briefly  recall  some  of  the  characteristic  symptoms  of 
the  chief  neuroses — neurasthenia,  psychasthenia,  and  hysteria — and 
note  in  what  respects  they  differ,  if  at  all,  from  analogous  symptoms 
produced  by  gross  organic  diseases. 

The  syndrome  known  as  Neurasthenia  or  nervous  exhaustion 
is  not  a  primary  disease.  It  is  exogenous,  the  result  of  something 
else.  The  commonest  cause  is  over-strain,  mental  or  physical, 
combined  with  some  emotion  of  a  disagreeable  kind.  It  may  also 
be  produced  by  excess  in  drugs  such  as  alcohol,  tobacco,  or  cocaine  ; 
or,  again,  by  the  toxins  of  various  infective  diseases  such  as  influ- 
enza, enteric  fever,  &c.,  or  by  the  auto -intoxication  associated 
with  dilatation  of  the  stomach  or  with  other  forms  of  gastro- 
intestinal disease.  Or  neurasthenia  may  result  from  organic  dis- 
eases, whether  these  be  of  the  nervous  system  {e.g.  tabes,  dissemi- 
nated sclerosis)  or  of  other  systems  (as  in  gout,  rheumatism,  cancer, 
and  so  on).  Eye-strain  from  uncorrected  astigmatism  is  a  common 
cause  which  is  frequently  overlooked.  Lastly,  a  particularly 
frequent  cause  is  traumatism,  especially  in  railway  accidents  which 
produce  a  common  type  of  neurasthenia  including  the  so-called 
"  railway  spine."     The  worry  and  uncertainty  of  Htigation  after 


380  NERVOUS    DISEASES 

accidents  of  this  sort  are  often  an  aggravating  factor,  both  in 
traumatic  neurasthenia  and  in  traumatic  hysteria.  Patients  with 
a  low  power  of  resistance  are,  of  course,  specially  hable  to  become 
neurasthenic  from  any  accidental  cause,  but  we  must  remember 
that  even  healthy  individuals,  without  neuropathic  taint,  may  be 
rendered  neurasthenic  as  a  result  of  over-strain  or  trauma  plus 
emotion. 

The  symptoms  of  neurasthenia  are  chiefly  subjective.  The 
patient  complains  of  undue  fatigue  and  feebleness  of  attention, 
so  that  sustained  mental  effort  becomes  impossible — so-called 
"  brain  fag."  There  is  "  irritable  feebleness  "  and  loss  of  emotional 
control,  with  general  gloominess  and  depression  of  the  whole  nervous 
system.  Painful  and  disagreeable  sensations  are  felt  too  acutely, 
whilst  the  reaction  to  pleasurable  emotions  is  diminished.  The 
patient's  memory  is,  however,  unimpaired,  and  he  relates  his  woes 
with  great  wealth  of  detail.  He  is  full  of  aches  and  pains,  but  on 
physical  examination  there  is  nothing  to  be  made  out  in  the  way 
of  anaesthesia  or  of  true  motor  paralysis. 

Amongst  the  motor  symptoms,  the  chief  is  muscular  asthenia 
or  excessive  tendency  to  fatigue,  so  that  every  movement  requires 
a  painful  effort  of  volition.  When  this  affects  the  internal  ocular 
muscles  it  constitutes  asthenopia  or  tiredness  of  the  eyes  on  attempt- 
ing to  accommodate  as  in  reading.  The  tongue  and  hmbs  are 
often  tremulous.  But  there  is  never  a  true  motor  paralysis.  Indi- 
vidual movements,  although  they  may  be  feeble,  tremulous,  and 
associated  with  an  intense  feeling  of  fatigue,  are  never  impossible. 
The  sense  of  fatigue  in  a  neurasthenic  patient,  unlike  hysteria,  is, 
as  a  rule,  uninfluenced  by  suggestion. 

The  sensory  symptoms  of  neurasthenia  include  subjective 
sensations  ad  infinitum,  all  of  them  disagreeable.  Pains  and 
dysaesthesiae  of  various  sorts  are  specially  common  in  the  head 
and  along  the  vertebral  column. 

Cardio -vascular  symptoms  are  common,  including  palpitation 
and  a  curious  violent  pulsation  of  the  abdominal  aorta,  which 
may  feel  almost  subcutaneous.  The  patient  often  complains  of 
sudden  flushes  of  heat  or  cold  traversing  the  trunk,  limbs,  or  face, 
also  of  paroxysmal  sweating,  and  so  on.  Sometimes  we  can  see 
transient  blotches  of  redness  at  the  sides  of  the  neck,  spreading 
upwards  over  the  angles  of  the  mandibles  on  to  the  cheeks.  Gastro- 
intestinal atony  is  common,  with  anorexia,  almost  invariably  gastric 


THE    NEUROSES  381 

dilatation,  dyspepsia,  and  constipation.  An  element  of  auto- 
intoxication is  thus  superadded,  which  aggravates  the  general 
malnutrition.  Sexual  disturbances,  e.g.  frequent  seminal  emissions, 
premature  ejaculations,  deficient  erections,  &c.,  are  not  uncommon, 
and,  when  present,  they  loom  large  in  the  mind  of  the  patient,  who 
exaggerates  their  importance  and  misinterprets  their  significance. 

The  superficial  reflexes  may  be  exaggerated,  especially  the  ab- 
dominal reflexes.  Sometimes  if  we  stroke  the  abdomen  in  a  circular 
direction  the  umbiUcus  moves  so  smartly  that  it  seems  to  be  chasing 
our  finger  round.  The  knee-jerks  in  neurasthenia  are  sometimes 
abnormally  brisk  and  accompanied  by  a  sudden  feeling  of  shock  in 
the  spine,  making  the  patient  start.  True  ankle-clonus,  however, 
does  not  occur,  and  the  plantar  reflexes,  if  present,  are  of  the  normal 
flexor  type.  The  sphincters  are  unaffected.  Most  neurasthenics 
are  poorly  nourished,  but  not  all  of  them. 

Psychasthenia  is  a  much  more  serious  affection,  in  which  the 
mental  phenomena  overshadow  the  physical.  Unlike  neurasthenia, 
which  is  usually  a  disease  of  adult  life  resulting  from  some  extraneous 
cause,  psychasthenia  is  an  endogenous  disease,  the  culmination 
of  an  ingrained  neuropathic  heredity,  and  its  earliest  indications 
appear  in  adolescence  or  even  in  childhood.  In  short,  the  psych- 
asthenic, like  the  poet,  is  "  born,  not  made."  Moreover,  while  neur- 
asthenia is  an  eminently  curable  afiection,  the  psychasthenic  patient 
remains  psychasthenic  all  his  life,  though  his  symptoms  may  be 
in  abeyance. 

The  outstanding  symptoms  of  psychasthenia,  as  Janet  has 
emphasized,  are  the  psychasthenic  "  stigmata,"  the  obsessions, 
and  the  imperious  acts.  The  stigmata  of  psychasthenia  may 
be  psychical  or  physical.  The  psychical  stigmata  of  psych- 
asthenia are  mental  anergia  and  irresolution.  The  psychasthenic 
feels  himself  incapable  of  fixing  his  attention,  whether  for  physical 
or  mental  effort ;  he  has  a  feeling  of  general  hesitation  and  doubt, 
and  has  to  lean  for  moral  support  on  others  possessing  a  stronger 
character  than  his  own.  This  anergia  or  defective  will-power  in 
psychasthenia  differs  from  the  anergia  of  true  melanchoha  in  that 
the  psychasthenic  is  distressed  by  his  anergia,  and  whilst  desirous 
to  act,  finds  himself  unable  to  do  so,  despite  extraordinary  and 
even  agonising  efforts.  The  melancholic  patient,  on  the  other  hand, 
is  not  merely  anergic  but  also  apathetic,  and  his  failure  to  act  causes 
him  little  or  no  distress.     Sometimes  the  psychasthenic  has  a  feeling 


382  NERVOUS    DISEASES 

of  double  personality,  in  which  he  feels  as  if  he  had  two  co-existing 
"egos."  The  double  personality  of  psychasthenia  differs  from  that 
of  hysteria,  in  which  the  duality  is  an  alternating  one,  as  a  rule 
unknown  to  the  patient. 

The  physical  stigmata  of  psychasthenia  are  evidenced  in  the 
patient's  actions.  Everything  he  does  tends  to  be  clumsy  and 
gauche  ;  his  very  gait  may  be  ungainly  ;  sometimes  he  is  a  stam- 
merer ;  he  is  often  a  "  liqueur  "  ;  he  is  full  of  affectations  and 
mannerisms.  In  addition  he  may  have  numerous  neurasthenic 
symptoms,  amongst  which  all  sorts  of  cephalic  sensations  are 
specially  common,  e.g.  sensations  of  fulness  or  emptiness  in  the 
head,  of  looseness  or  tightness,  of  creaking  or  sawing,  and  so 
on.  Physical  or  mental  over-exertion  or  excitement  may  even 
induce  an  epileptiform  fit.  Gastro -intestinal  atony  is  common, 
with  all  its  train  of  symptoms  in  the  form  of  dyspepsia,  consti- 
pation, &c.  ;  the  circulatory  and  vaso-motor  systems  may  be 
affected,  e.g.  by  paroxysms  of  palpitation,  attacks  of  blushing 
or  pallor,  excessive  sweating  or  abnormal  dryness  of  the  skin ; 
the  sexual  functions  are  usually  diminished,  in  male  patients 
spermatorrhoea  is  particularly  common,  and,  as  in  neurasthenia, 
the  general  nutrition  is  usually  below  par. 

The  second  great  characteristic  of  psychasthenia  is  the  presence 
of  systematised  obsessions  or  dominant  ideas  of  various  sorts.  These 
are  almost  always  of  a  depressing  type  and  may  be  of  the  most 
varied  forms.  A  psychasthenic  obsession  comes  on  spontaneously 
in  paroxysms  and  cannot  be  inhibited  by  any  effort  of  the  patient. 
When  the  obsession  arrives,  it  occupies  the  patient's  entire  atten- 
tion, so  that,  for  the  time,  he  can  think  of  nothing  else.  In  the  in- 
tervals between  his  paroxysms  the  psychasthenic  is  a  fairly  normal 
person,  taking  an  interest  in  the  ordinary  incidents  and  pleasures 
of  life.  In  this  respect  he  differs  essentially  from  the  melancholic, 
whose  depression  is  continuous,  who  lives  in  constant  gloom  and 
derives  no  pleasure  from  life.  Although  the  obsession  is  often 
an  idea  which  is  repulsive  to  the  patient,  yet  it  is  most  insistent 
and  tends  to  recur  again  and  agam.  The  patient  recognises  it  as 
being  a  morbid  idea,  yet  he  cannot  throw  it  off.  The  different 
obsessions  vary  in  their  tendency  to  become  translated  into  actions. 
Thus,  though  psychasthenics  often  have  obsessions  of  suicide,  they 
very  rarely  attempt  suicide  ;  on  the  other  hand  obsessions  to  steal 
(kleptomania),  to  drink  (dipsomania),  and  to  perform  sexual  acts 


THE    NEUROSES  383 

are  more  difficult  to  resist.  A  certain  proportion  of  professional 
"  tramps  "  are  simply  psychasthenic  individuals  obsessed  by  the 
impulse  to  wander  from  place  to  place,  unable  to  settle  down,  even 
when  offered  the  work  for  which  they  profess  themselves  to  be 
looking.  We  should  note  that  though  the  psychasthenic  patient 
may  have  obsessions,  he  has  no  delusions  or  hallucinations ; 
reasoning  powers  are  unimpaired.  He  must  therefore  be  clearly 
distinguished  from  the  insane  patient. 

The  third  characteristic  feature  of  psychasthenia  is  the  occur- 
rence of  imferious  acts  {i.e.  an  irresistible  tendency  to  perform 
some  special  act),  and  of  paroxysmal  imperious  ideas.  Imperious 
acts  include  the  innumerable  varieties  of  tics  (see  pp.  100-102).  As 
to  the  paroxysmal  imperious  ideas,  these  include  such  varieties  as 
the  mania  for  perpetually  asking  questions  {folie  de  fourquoi),  the 
mania  of  fussy  tidiness,  the  mania  of  counting  things  over  and  over 
{arithmomania),  the  mania  of  searching  for  objects,  and  so  on. 
Manias  of  this  sort,  of  course,  interfere  with  normal  mental  pro- 
cesses, interrupting  them  to  such  an  extent  that  the  patient  finishes 
by  accomplishing  practically  nothing  in  the  way  of  mental  work. 
Imperious  ideas  may  also  be  of  an  emotional  nature  ;  these  include 
the  innumerable  forms  of  phobia,  such  as  agoraphobia  (fear  of  being 
in  open  spaces),  claustrophobia  (fear  of  being  inside  shut  doors, 
especially  of  public  buildings),  anthropophobia  (fear  of  crowds), 
monophobia  (fear  of  being  alone),  aichmophobia  (fear  of  sharp 
objects),  rupophobia  (fear  of  dirt),  toxicophobia  (fear  of  being 
poisoned),  ereutophobia  (fear  of  blushing),  fear  of  darkness,  fear  of 
death,  fear  of  illness,  fear  of  performing  organic  functions  such 
as  micturition  or  defaecation  (coprofhohia),  unreasonable  fear  of 
certain  animals  or  insects,  and  so  on,  ad  infinitum.  In  most  of 
these  psychasthenic  phobias  there  is,  coexistent  with  the  repul- 
sion for  the  particular  act  or  object,  a  strong  attraction  to  that 
same  object  or  act.  This  mixture  of  apprehension  and  attraction, 
as  Raymond  ^  has  pointed  out,  is  one  of  the  causes  of  the  mental 
agitation  which  accompanies  a  psychasthenic  phobia. 

Lastly,  we  come  to  the  subject  of  Hysteria.  This  is  a  disease 
which  is  much  commoner  in  women  than  in  men.  It  is  more 
frequent  during  adolescence  and  adult  life  than  in  childhood  or 
old  age,  although  it  may  sometimes  occur  in  little  children  of  8,  6, 
or  even  4  years.     Whilst  no  race  and  no  people  is  exempt  from 

1  Bulletin  Medicale,  1907,  No.  30. 


384  NERVOUS    DISEASES 

hysteria,  it  is  relatively  more  frequent  in  the  Latin  races  and 
amongst  the  Jews.  Many  cases  of  hysteria  have  a  nervous  heredity. 
Hysterical,  alcoholic,  or  tuberculous  parents  are  prone  to  have 
hysterical  children.  We  frequently  find  physical  or  emotional 
shocks  as  exciting  causes,  or  a  combination  of  the  two,  as  for 
example  after  a  shell -explosion  during  battle,  an  earthquake,  a 
stroke  of  lightning,  an  electric  shock,  or  a  railway  accident,  especially 
if  this  latter  be  followed  by  litigation.  Imitation  of  other  hysterics 
may  produce  epidemics  of  hysteria,  whether  in  adolescents  as  in  girls' 
schools,  or  in  adults  as  in  certain  religious  "  revival  meetings." 

In  some  cases  there  is  a  sexual  element  in  the  causation,  though 
probably  less  constantly  than  Freud  and  his  followers  would  have 
us  believe.  According  to  Freud's  hypothesis,  hysteria  and  other 
psycho -neuroses  are  supposed  to  be  due  to  "  repression  "  of  some 
old  emotional  trauma,  usually  of  a  sexual  character.  At  the  time 
of  the  original  emotional  incident,  the  feeling  to  which  it  gives  rise, 
instead  of  gaining  vent,  as  in  health,  either  in  satisfaction  of  the 
desire  or  in  vigorous  refusal  to  yield  to  it,  is  supposed,  in  the  hys- 
terical individual,  to  become  repressed  or  thrust  back  into  the 
patient's  subconscious  memory,  thenceforward  gaining  expression 
from  time  to  time  in  an  abnormal  fashion  under  the  guise  of  some 
nervous  symptom  or  some  phobia  or  obsession.  If  this  "  repressed  " 
trauma,  this  skeleton  in  the  secret  cupboard  of  the  mind,  can  by 
some  means  be  dragged  forth  to  the  patient's  consciousness,  the 
hysterical  symptom  is  supposed  to  become  dispersed,  by  a  process 
of  "  mental  catharsis,"  so  that  conscious  control  is  substituted  for 
automatic  expression.  Believers  in  this  theory  proceed  to  "  dig 
up"  the  original  trauma  by  the  process  of  so-called  "psycho- 
analysis." This  consists  in  a  detailed  scrutiny  of  the  patient's 
past  history,  from  childhood  onwards,  so  as  to  try  and  identify 
the  precise  circumstances  under  which  the  symptom  first  arose. 
For  this  purpose  Jung's  word-association  method  is  employed,  in 
which  a  long  series  of  test-words  (stimulus-words),  consisting  of 
carefully-selected  nouns,  verbs,  and  adjectives  in  everyday  use 
(of  which  a  certain  number  have  been  specially  selected  in  view  of 
the  physician's  previous  study  of  the  patient), ^  are  one  by  one  read 

1  The  following  is  a  series  of  test-words  taken  from  Jones's  book: — ■ 
Coal,   brother,  mount,  tea,  drop,  cow,  pin,  blood,  tree,  snow,  rail,  plate, 
touch,  train,  roof,  rub,  bag,  watch,  jump,  mouse,  post,  blue,  pot,  stick,  chair, 
ball,  sheet,  egg,  wood,  note,  fire,  sister,  cup,  warm,  turn,  waste,  dog,  hand, 
tongs,  stone,  table,  ride,  paper,  room,  red,  live,  back. 


THE    NEUROSES  385 

to  the  patient,  who  has  been  previously  instructed  to  listen  atten- 
tively and  to  reply  to  each  test-word  with  the  very  first  word  or 
phrase  which  the  stimulus-word  suggests  to  his  mind  {e.g.  "  snake — 
poison,  pain — tears,  sister — darling,  yellow — hideous,"  &c.).     The 
physician  not  only  makes  a  note  of  the  response-word  given  to  each 
stimulus-word,  but  at  the  same  time,  by  means  of  a  stop-watch 
registering  fifths  of  a  second,  he  records  the  interval  of  time  in 
each  case  between  the  stimulus-word  and  the  reaction-word.     In 
ordinary  persons  the  average  reaction-time  is  from  six  to  twelve- 
fifths  of  a  second.     In  hysterical  patients  various  pecuHarities  in 
the  responses  indicate  the  existence  of  certain  trains  of  thought 
of  high  emotional  value,  so  that  the  patient  hesitates,  pauses,  or 
sticks  over  certain  words  in  the  list,  has  a  difficulty  in  responding, 
or  shows  other  abnormalities  of  response.     The  chief  peculiarities 
in  response  consist  in  undue  delay  in  reaction-time  with  certain 
test-words,  a  delay  which  may  amount  to  twice  or  three  times  the 
average  reaction-time  taken  for  the  other  test- words.     Or  there 
may  be  a  failure  to  respond  at  all,  or  a  senseless,  siUy  reaction,  or 
a  response  by  mere  repetition  of  the  test-word,  or  by  repeated 
use  of  the  same  response-word.     On  looking  through  the  com- 
pleted list  of  test-words,  reaction-times,  and  responses,  and  having 
discovered  one  or  two  peculiar  responses  of  this  sort,  the  psycho- 
analyst proceeds  to  cross-examine  the  patient  as  to  the  thread 
of  sub-conscious  thought  which  connects  the  stimulus-word  with 
the  delayed  or  peculiar  response- word.     This  thread,  in  Freudian 
hands,  always  proves  to  possess  a  sexual  continuity.     The  psycho- 
analyst of  the  Freudian  school  also  studies  the  patient's  dreams 
(which  are  supposed  to  represent  the  imaginary  gratification  of 
ego-centric  desires  that  have  undergone  repression  in  daily  life), 
and,  on  the  theory  that  the  latent  content  of  dreams  and  of  neurotic 
symptoms  is  always  of  a  sexual  nature,  he  submits  the  patient's 
dreams  to  similar  "  analysis  "  and  constructs  ingenious  compari- 
sons between  the  dream  and  the  patient's  symptoms. 

To  the  non-Freudian  physician  many  of  these  "  analyses " 
appear  prurient  and  far-fetched.  As  Jones  admits,  "  particularly 
with  the  more  complex  analyses,  doubt  must  always  arise  concern- 
ing the  trustworthiness  of  the  results."  ^  Freud  deserves  credit 
for  emphasizing  the  sexual  element  underlying  a  considerable 
proportion  of  cases  of  hysteria  and  of  other  psycho-neuroses,  but 

1  Ernest  Jones,  Psycho-Analysis,  London,  1913. 

2   B 


386  NERVOUS    DISEASES 

it  is  a  grotesque  exaggeration  to  attribute  every  case  of  neurosis 
to  a  trauma  of  purely  sexual  origin,  whilst  ignoring  innumerable 
other  sorts  of  traumata,  physical  or  emotional. 

Hysterical  states  shade  imperceptibly  into  normal  mental 
states,  there  being  no  hard  and  fast  line  of  demarcation.  A 
certain  susceptibility  to  suggestion  and  a  certain  emotional  re- 
action exist,  of  course,  in  normal  individuals  in  widely  varying 
degrees.  Such  phenomena  are  especially  marked  in  children.  In 
fact,  as  Schnyder  ^  has  said,  we  may  speak  of  the  "  physiological 
hysteria  "  of  childhood.  But  if  an  adult  reverts  to  the  childish 
susceptibility  to  suggestion  and  to  infantile  emotional  reactions, 
we  consider  him  or  her  pathological,  hysterical  in  fact. 

For  purposes  of  convenience  we  shall  consider  the  symptoms 
in  four  groups — psychical,  sensory,  motor,  and  lastly,  visceral  and 
vascular.  In  each  of  these  groups  we  may  find  excess,  diminution, 
or  perversion  of  the  normal  nervous  processes. 

Psychical  Symptoms. — These  are  invariably  present  in  hysteria 
to  a  greater  or  less  degree.  The  most  outstanding  feature  is 
deficiency  of  inhibition  or  psychical  instability.  The  patient  reacts 
too  readily  to  stimuli  or  suggestions,  whether  originating  in  the 
outside  world  or  within  her  own  body.  One  of  the  most  striking 
instances  of  this  is  found  in  the  phenomena  of  hypnotic  suggestion, 
whereby  a  peculiar  form  of  temporary  hysteria — the  hypnotic 
trance — is  artificially  induced  by  suggestion,  and  can  be  made 
suddenly  to  disappear  by  the  same  means.  This  disappearance 
of  symptoms  during  or  after  hypnosis  is  sometimes  taken  advantage 
of  in  the  treatment  of  hysteria  by  hypnotic  suggestion.  It  is 
open  to  the  objection  that,  instead  of  strengthening  the  patient's 
feeble  inhibition,  it  temporarily  multiplies  that  fault.  Yet  if  the 
result  be  that  the  patient  has  a  hysterical  suppression  of  her  hys- 
terical symptoms  or  an  inhibition  of  the  inhibitory  centres  (on  the 
mathematical  principle  that  —  x  —  =  +  )  it  is,  none  the  less,  of 
therapeutic  value.  But  results  obtained  by  this  plan  are  less  likely 
to  be  permanent  than  when  we  strengthen  the  patient's  inhibition 
or  self-control  by  positive  measures. 

Deficient  inhibition  being  the  keynote  of  the  hysterical  "  V^i^x?;," 
we  find,  accordingly,  that  the  patient  is  excessively  emotional, 
unstable,  and  changeable  in  disposition,  often  excitable  and  perhaps 
passionate.     She  giggles  or  cries  on  slight  provocation,  and  one  of 

^  Journal  de  Neurologic,  1907,  p.  281. 


THE    NEUROSES 


387 


the  most  familiar  forms  of  hysterical  "  fit "  consists  merely  in 
alternate  loud  laughter  and  crying.  Her  will-power  is  feeble,  her 
mental  field  of  vision  is  narrowed,  and  she  is  morbidly  introspective 
and  swayed  by  passing  whims  ;  and  this  want  of  self-reliance  leads 
to  another  very  characteristic  symptom — the  craving  for  sympathy. 
If  that  sympathy  be  shown,  as  is  so  often  the  case,  to  an  injudicious 
extent  by  the  patient's  relatives  and  friends,  her  recovery  may 
be  indefinitely  delayed.  Hence  it  is  generally  of  supreme  im- 
portance to  remove  the  hysterical  patient  completely  from  her 


Figs.  197  and  197a.  — Case  of  hysterical  paraplegia  of  fourteen  years' 
duration.  Showing  a  characteristic  hysterical  posture  of  the  feet 
when  the  patient  is  passively  supported. 


old  surroundings,   and  to   isolate  her  until  the  vicious   circle  is 
broken. 

Figs.  197  and  197a  are  photographs  of  a  woman  aged  37, 
who  for  over  fourteen  years  had  lain  on  a  bed  of  sickness 
unable  to  move  her  legs,  a  case  of  hysterical  paraplegia.  But 
she  was  cherished  by  the  sympathy  of  a  devoted  mother 
and  of  various  benevolent  lady- visitors,  anxious  to  soothe 
her  dying  moments.  She  was  admitted  to  hospital,  and  as  a 
result  of  six  weeks  of  isolation  and  massage,  she  recovered  the 
power    of  walking,   as   will  be  seen   from    the   other  photograph 


388 


NERVOUS    DISEASES 


(Fig.    198).      This   successful  result  was   due  quite   as  much   to 
the  isolation  and  psychical  treatment  as  to  the  other  measures, 

such  as  special  diet,  and  mas- 
sage. 

It  is  convenient  to  men- 
tion here,  in  connection  with 
the  psychical  symptoms,  the 
hysterical  affections  of  speech. 
Sometimes  there  is  excessive 
volubility — a  diarrhoea  verbo- 
rum.  In  other  cases  we  find 
the  reverse  condition  of  hys- 
terical mutism,  in  which  the 
patient  is  absolutely  dumb. 
Hysterical  aphasia  usually 
deviates  in  some  gross  or 
paradoxical  fashion  from  or- 
ganic aphasia.  It  is  often 
accompanied  by  curious  tricks 
of  pronunciation  or  of  into- 
nation. In  less  severe  cases 
it  is  not  uncommon  to 
find  merely  loss  of  voice,  or 
hysterical  aphonia — where  the 
patient  can  only  utter  her 
tale  of  woe  in  a  whisper, 
breathing  it  softly  into  the 
ear  of  a  sympathetic  listener. 
Hysterical  aphonia  has  char- 
acteristic laryngoscopic  ap- 
pearances, in  the  form  of  ad- 
ductor paralysis  of  the  cords, 
with  which  we  are  familiar. 

Patients  with  mutism  or 
aphonia  sometimes  suddenly 
recover  their  voice  when  the  dominant  obsession  is  loosened, 
e.g.  by  administration  of  chloroform  (by  the  physician),  or  of  an 
excess  of  alcohol  (by  the  patient),  or  by  some  sudden  shock, 
physical  or  mental.  Intra-laryngeal  faradism  cures  immediately 
many  cases  of  hysterical  aphonia. 


Fig.  198. — The  same  patient  as  in  Figs. 
197  and  197a,  after  six  weeks'  treat- 
ment, showing  restoration  of  power 
of  walkinar. 


THE    NEUROSES  389 

Articulation  in  hysterical  and  psychasthenic  patients  may 
be  affected  in  all  sorts  of  curious  fashions.  I  have  seen  seve- 
ral patients  who  drew  a  breath  after  each  separate  syllable, 
e.g.  "  hos — pi — tal."  .Some  psychasthenic  "  tiqueurs  "  interpolate 
curious  barking,  grunting,  or  snorting  noises  amongst  their 
words.  One  lady  was  afflicted  in  this  way  to  such  an  extent 
that  new  neighbours  who  settled  in  an  adjoining  house  thought 
the  noise  was  made  by  a  sick  dog,  and  made  a  humane  suggestion 
that  the  animal  should  be  put  out  of  its  pain.  And  yet  this 
lady  could  recite  long  dramatic  passages  of  poetry  and  prose, 
though  in  ordinary  conversation,  or  even  when  not  talking,  her 
bark  made  her  society  a  mixed  pleasure. 

Stammering  in  its  difierent  varieties  is  not  uncommon  in 
hysterical  and  psychasthenic  individuals.  Unlike  ordinary  stam- 
mering which  comes  on  in  childhood,  hysterical  stammering  may 
develop  suddenly  in  adult  hfe.  Thus  in  a  hospital  nurse  aged  33, 
who  stood  up  sharply  and  knocked  her  head  against  a  mantel- 
shelf, severe  hysterical  hemiplegia  came  on  next  day,  and,  some 
six  weeks  later,  stammering,  which  lasted  for  several  months. 

Sensory  Symptoms. — These  are  of  greater  diagnostic  import- 
ance than  is  commonly  reahsed.  Pain  of  some  sort  occurs  in  nearly 
every  case  of  neurasthenia  and  in  many  cases  of  hysteria.  Unhke 
ordinary  pains,  which  are  generally  caused  by  some  peripheral 
irritation,  hysterical  and  neurasthenic  pains  are  entirely  central 
in  origin — psychalgia — and  should  really  be  classed  as  halluci- 
nations. But  in  every  case  we  must  be  careful  to  see  and  to 
examine  the  painful  spot,  and  to  exclude  peripheral  irritation, 
before  labelhng  any  pain  as  hysterical  or  neurasthenic. 

Hysterical  fains  may  be  referred  to  any  part  of  the  body ;  but 
they  are  especially  common  in  certain  situations.  For  example, 
hysterical  headache  is  often  of  the  "  clavus  "  type,  which  is  a 
boring  pain  localised  to  one  small  spot  on  the  skull.  Occipital 
headache  is  particularly  common,  so  is  hemicrania.  Pains  in  the 
spine  may  simulate  those  of  organic  disease.  Pain  in  the  breast 
— mastodynia — or  in  the  joints  may  lead  to  difficulties  in  diagnosis. 
It  is  only  by  careful  local  and  general  examination,  revealing  the 
presence  of  other  hysterical  stigmata  and  the  absence  of  signs 
of  structural  disease,  that  we  can  avoid  errors.  Cases  have  been 
known  in  which  amputations  have  been  performed  for  hysterical 
joint-pains.     Some  time  ago  I  saw  a  young  lady  who  had  already 


390  NERVOUS   DISEASES 

had  one  toe  removed   by   a  surgeon,   but  the  pain  recurred  in 
another  toe,  and  the  case  was  undoubtedly  hysterical. 

Closely  related  to  these  pains  are  the  areas  of  hysterical  hyper- 
cesihesia,  and  especially  of  hyperalgesia  or  excessive  tenderness. 
Pain  on  pressure  over  certain  spots,  whether  such  pain  be  functional 
(hysterical  or  neurasthenic)  or  organic  in  origin,  has  occasionally  to 
be  differentiated  from  the  simulated  tenderness  of  a  malingerer.  In 
such  cases  Mannkopfs  sign  is  sometimes  useful.  This  consists  in  a 
change  in  the  pulse-rate  whilst  the  painful  spot  is  being  pressed 
upon — usually  a  temporary  acceleration  of  from  10  to  30  beats 
per  minute.  This  is  common  in  functional  cases.  Sometimes,  on 
the  other  hand,  the  pulse  is  slowed,  especially  in  cases  of  scars  from 
organic  injuries.^  In  cases  of  malingering,  however,  no  alteration 
in  the  pulse-rate  is  produced. 

Universal  hypersesthesia  occurs,  though  rarely,  and  we  also  meet 
with  cases  of  hemi-hyperaesthesia.  More  usually  this  excessive 
tenderness  is  limited  to  small  areas — little  islands  of  skin  or  sub- 
jacent tissues  of  the  head,  trunk,  or  limbs.  Sometimes  the 
tenderness  is  cutaneous  and  ehcited  by  gentle  stroking  of  the  skin  ; 
sometimes  it  is  subcutaneous,  and  only  elicited  on  deeper  pressure. 

Such  tender  points  are  chiefly  situated  in  the  vertebral,  infra- 
mammary,  epigastric,  and  inguinal  regions,  and  except  when 
mesial,  are  more  frequently  left-sided  (except  in  left-handed  people, 
in  whom  they  are  more  commonly  right-sided).  Tender  points  are 
less  common  on  the  head,  and  rarest  on  the  Hmbs.  Graves  '^  has 
directed  attention  to  the  frequent  presence,  in  hysterics  of  either 
sex,  of  hyperalgesia  to  pin-pricks  together  with  tactile  anaesthesia, 
confined  to  the  nipples  and  their  areolae. 

Of  all  the  tender  spots,  that  in  the  left  inguinal  region  is  per- 
haps the  commonest.  From  some  supposed  connection  with  the 
ovary,  it  has  been  called  "  ovarian  "  tenderness,  but  the  symptom 
is  as  frequent  in  male  hysterics  as  in  females,  so  that  the  term 
is  a  misnomer.  Moreover,  in  this  connection,  Steinhausen  ^ 
examined  500  healthy  soldiers — males,  not  Amazons — and  found 
that  in  no  less  than  88  per  cent,  brisk  pressure  in  the  inguinal 
region  on  either  side  produced  a  reaction  of  some  sort,  the  pheno- 
mena being  either  sensory  (unpleasant  tickling  or  pain),  motor 

^  Hudovernig,  Neurolog.  Gentralhl.,  1910,  s.  408. 
^  Journal  of  Nervous  and  Mental  Diseases,  October  1905. 
'  Steinhausen,   Ueber  die  physiologische  Grundlage  der  hysterischen  Ovarie. 
Deutsche  Zeitsch.  f.  Nervenheilk.,  xix.  s.  369. 


THE    NEUROSES  391 

(hardening  of  abdominal  muscles,  various  reflex  and  protective 
movements),  psychical,  or  vaso-motor  and  sympathetic  (dilatation 
of  pupils).     And  yet  there  was  not  a  single  ovary  amongst  them. 

These  tender  points  may  be  associated  not  merely  with  pain, 
but  with  so  much  disturbance  as  to  be  actually  hysterogenic.  This 
does  not  mean  that  they  induce  hysteria — the  hysteria  is  already 
present.  It  means  that  pressure  on  such  a  spot  induces  a  hysterical 
fit  or  paroxysm.  The  best-known  hysterogenic  area  is  in  the  left 
inguinal  region,  but  such  areas  may  be  anywhere.  I  know  of  one 
patient  who  had  a  hysterogenic  spot  in  one  axilla  and  who  wore 
a  sort  of  truss  over  it,  to  prevent  accidental  pressure. 

Sometimes  deeper  pressure  on  the  hysterogenic  spot  or  else- 
where may  arrest  a  hysterical  fit  when  in  progress.  Areas,  pressure 
upon  which  causes  cessation  of  the  paroxysms,  are  called  hjstero- 
frenic.  The  inguinal  region  is  the  best  known  of  these.  Strong 
faradism  over  the  inguinal  region  will  stop  most  hysterical  fits  ; 
so  also  will  a  hypodermic  injection  of  apomorphine  with  its 
resultant  vomiting. 

Hysterical  hypersesthesia  may  also  affect  the  special  senses,  so 
that  there  may  be  hyper-sensitiveness  of  smell,  vision,  hearing, 
or  taste.  This  is  less  common  than  loss  or  diminution  of  special 
senses,  to  which  we  shall  refer  later.  For  some  time  I  had  under 
my  care  a  patient  who  could  not  tolerate  bright  light,  especially 
if  the  room  had  a  blue  wall-paper.  He  preferred  to  stay  in  a 
darkened  chamber ;  or  if  the  bhnds  were  up,  he  shaded  his  eyes 
with  his  hand.  After  some  weeks  of  treatment,  he  completely 
lost  this  photophobia. 

In  rare  cases  an  actual  enlargement  of  the  visual  field  has 
been  observed,  generally  in  one  eye  only.  Thus,  in  a  soldier  with 
hysterical  wry-neck  and  anassthesia  of  one  side  of  the  body,  the 
visual  field  on  the  non-ansesthetic  side,  when  measured  with  the 
perimeter,  was  much  larger  than  in  a  normal  individual. 

Hysterical  anwsthesia  is  extremely  common,  and  is  of  the  greatest 
diagnostic  value.  A  degree  of  anaesthesia  exists,  I  am  convinced, 
in  the  overwhelming  majority  of  hysterical  cases,  except  those 
occurring  in  childhood.  Some  time  ago  I  looked  through  my  notes 
of  63  consecutive  cases  and  found  that  anaesthesia  was  present  in 
50  and  absent  only  in  12.  The  remaining  case  of  the  series  had 
unilateral  hypersesthesia. 

Hysterical  anaesthesia  is  usually  unnoticed  by  the  patient  her- 


392  NERVOUS    DISEASES 

self,  and  only  discovered  on  examination  by  the  physician.^  Some- 
times, however,  the  patient  complains  of  actual  numbness,  and 
this  is  chiefly  in  cases  when  the  affected  limb  has  motor  paralysis 
as  well,  so  that  her  attention  is  called  to  it. 

Janet  showed  an  ingenious  method  of  demonstrating  that 
in  some  cases  of  hysterical  anaesthesia,  sensory  impulses  really 
reach  the  brain-centres,  though  the  patient  does  not  consciously 
perceive  them.  Taking  a  case  of  complete  hemi-ansesthesia  he 
makes  the  patient  shut  her  eyes,  and  tells  her  to  say  "  Yes  " 
each  time  she  feels  a  touch  or  prick,  and  to  say  "  No  "  when  she 
does  not  feel  it.  In  certain  cases  the  patient  not  only  says  "  Yes  " 
every  time  she  is  touched  on  the  normal  side,  but  also  says  "  No  " 
every  time  she  is  touched  upon  the  anaesthetic  side.  In  other 
words,  the  patient  feels,  though  she  does  not  know  that  she  feels. 
This  is  pathognomonic  of  hysteria. 

Cutaneous  anaesthesia  in  hysteria  may  be  complete  or  partial 
in  degree,  or  it  may  be  dissociated.  Diminution  or  loss  of  painful 
sensations  is  even  commoner  than  tactile  anaesthesia.  Many  of 
the  mediaeval  witches  were  simply  hysterics.  Their  hysterical 
analgesia  (sigillum  diaboli)  was  usually  demonstrated  by  sticking 
pins  into  them,  and  if  an  analgesic  area  was  discovered,  they  were 
promptly  thrown  into  the  nearest  pond  or  stream.  If  they  sank 
and  were  drowned,  their  innocence  was  established ;  but  if  they 
floated,  it  was  additional  evidence  of  guilt. 

Whatever  be  its  degree  of  intensity,  hysterical  anaesthesia 
never  maps  out  an  individual  nerve-area  such  as  that  of  the  radial, 
median,  ulnar,  or  external  popliteal.  Its  commonest  distribution 
is  a  hemi-ancesthesia  (27  out  of  50  cases)  which  is  mostly  left-sided, 
except  in  left-handed  patients.  It  is  a  remarkable  fact  that  a 
hysterical  patient  never  suffers  any  physical  disability  owing  to 
the  existence  of  anaesthesia,  no  matter  how  profound.  Unlike  a 
patient  with  organic  anaesthesia,  the  hysteric  never  cuts  or  burns 
herself  unconsciously  in  an  anaesthetic  area. 

1  Babinski  considers  that  hysterical  anaesthesia  is  mainly  the  result  of 
suggestion  by  the  examining  physician.  With  this  view  I  cannot  agree. 
Many  patients  who  are  highly  susceptible  to  suggestion  have  no  anaesthesia. 
Moreover,  undoubted  cases  of  hemi-ansesthesia  have  been  known  to  develop 
before  any  medical  examination  had  taken  place,  the  anaesthesia  being  dis- 
covered accidentally  either  by  the  patient  or  by  some  lay  observer.  Moreover, 
why  pick  out  sensory  symptoms  and  say  that  they  are  suggested  by  the  physi- 
cian ?  Why  not  include  motor  symptoms  also  ?  Why  not  all  the  symptoms  ? 
If,  as  Babinski  admits,  the  patient  is  capable  of  producing  his  motor  symptoms 
by  auto-suggestion,  why  can  he  not  produce  sensory  symptoms  at  the  same  time? 


THE    NEUROSES 


393 


Myi 


Fig.  199.— Various  types  of  hysterical  antesthesia.  Dotted  areas  indicate  slight 
sensory  loss,  shaded  areas  more  severe  impairment,  and  black  areas  total  loss 
of  sensation. 


394 


NERVOUS    DISEASES 


Nowli 


Fig.  200.— Case  of  hysterical  paralysis  in  a  girl  aged  17,  showing 
progressive  improvement  in  the  anaesthesia. 


THE    NEUROSES 


395 


Hysterical  hemi-ansBsthesia,  including  the  accessible  mucous 
membranes  of  the  eye,  nose,  mouth,  pharynx,  vagina  and  rectum, 
is  usually  accurately  bounded  by  the  middle  line  ;  but  not  always. 
It  may  either  extend  farther  over  and  encroach  on  the  non-anaes- 
thetic side,  or  it  may  leave  certain  areas  with  normal  sensation, 
even  on  its  own  side,  especially  the  head,  the  nipple,  and  the 
genitals,  as  may  be  seen  from  the  charts  (Figs.  199  and  200). 

n 


Fig.  201. — Case  of  hysterical  paralysis  in  a  left-handed  patient, 
showing  progressive  improvement  in  anaesthesia. 

Bilateral  universal  anaesthesia  is  rare  (see  Fig.  87,  p.  207). 
We  generally  find,  somewhere  or  other,  one  or  more  islands  of 
normal  sensation,  or  even  of  hyper-sensitiveness.  Pharyngeal 
anaesthesia  is  one  of  the  commonest  hysterical  stigmata.  It  is 
not  necessarily  accompanied  by  loss  of  the  pharyngeal  reflex. 

In  many  cases  the  anaesthesia,  though  unilateral,  is  more  marked 
on  the  face  or  limbs  than  on  the  trunk.  It  may  affect  special 
levels  of  a  limb  (knee,  elbow,  or  shoulder),  or  it  may  stop  abruptly 


396 


NERVOUS    DISEASES 


at  some  horizontal  line  (shoe,  sock,  stocking,  mitten,  glove,  sleeve). 
This  "  segmental "  ancesthesia  sometimes  occurs  in  association  with 
hemi-ansesthesia  (10  out  of  50  cases)  or  by  itself  (12  out  of  50)  on 
one  or  both  sides  (Figs.  201  to  203). 

The  mode  of  onset  and  disappearance  of  hysterical  ansesthesia 
is  interesting.     Sometimes  the  anaesthesia  comes  on  gradually,  and 


Fig. 


202. — Case  of  hysterical  hemiplegia,  showing  variations  in 
anaesthesia. 


the  patient  is  unconscious  of  the  defect.  In  other  cases  it  occurs 
suddenly,  especially  after  a  hysterical  fit,  and  the  patient  is  then 
more  likely  to  notice  her  "  numbness." 

We  seldom  have  the  chance  of  watching  the  onset  of  hysterical 
anaesthesia,  but  we  may  often  study  its  mode  of  disappearance, 
and  Figs.  200  to  203  show  charts  of  several  cases  of  hysterical 
anaesthesia  in  various  stages  of  recovery.  Unlike  organic  anaesthesia, 
which,  if  recovered  from,  fades  gradually  all  over  the  recovering 
area,  hysterical  hemi-anaesthesia  may  suddenly  fade  to  segmental 


THE    NEUROSES 


397 


(Fig.  200),  and  segmental  anaesthesia  recedes  by  jumps  from  a 
higher  to  a  lower  level,  bounded  usually  by  an  "  amputation  line  " 
drawn  transversely  across  the  limb.  Sometimes  it  relapses  tempo- 
rarily to  its  old  level  before  resuming  its  progress  towards  recovery 
(Figs.  201  and  202).  More  rarely  it  clears  up  first  at  the  periphery. 
AncEsthesia  of  Special  Senses. — Most  cases  of  hysterical  anaes- 


FlG.  203. — Case  of  hysterical  paraplegia  with  anaesthesia  in  a  girl  aged  19, 
showingtprogressive  improvement. 


thesia  also  have  diminution  or  loss  of  the  special  senses — smell, 
vision,  taste,  and  hearing— generally  unilateral  and  on  the  same 
side  as  the  cutaneous  anaesthesia,  rarely  on  the  opposite  side. 
This  combination  of  unilateral  affection  of  special  senses  and  of 
cutaneous  sensation  is  pathognomonic  of  hysteria,  and  does  not 
occur  in  organic  disease. 

The  affection  of  vision  in  hysteria  is  not  a  hemianopia  such  as 
we  often  get  in  organic  hemiplegia.  It  is  a  concentric  contraction 
of  the  whole  visual  field,  as  will  be  seen  from  the  accompanying 


398 


NERVOUS    DISEASES 


perimetric  charts  (Fig.  204).  It  is  more  marked  in  one  eye 
than. in  the  other — "  crossed  amblyopia  " — the  smaller  field  being 
on  the  hemi- anaesthetic  side,  usually  the  left. 

Sometimes,  when  charting  the  visual  field  of  a  hystero-neuras- 


Crossed  amblyopia. 


Right  homonymous  hemianopia. 

Fig.  204. — Visual  fields  from  cases  of  hysterical  and  organic  hemiplegia 
respectively,  in  which  vision  was  affected. 

thenic  patient,  we  notice  that  the  field  becomes  progressively  smaller 
and  smaller  from  rapid  fatigue  as  we  continue  our  examination ; 
so  that  our  perimetric  outline  has  a  helicoid  or  spiral  shape  (Fig.  205). 
This  form  of  perimetric  tracing  does  not  occur  in  organic  disease. 

Sometimes  we  have  hysterical  bhndness  or  apparent  amaurosis 
in  one  eye,  and  yet  by  means  of  prisms  we  may  produce  diplopia. 


THE    NEUROSES 


399 


a  condition  of  affairs  which  would  be  impossible  in  an  organic  case. 
In  rare  cases  complete  bilateral  hysterical  blindness  has  been 
observed. 

Perhaps  the  most  striking  variety  of  hysterical  blindness  is  the 
traumatic  amblyopia  which  sometimes  follows  the  bursting  of  a 
high-explosive  shell.  The  patient  is  usually  concussed,  and  may 
even  be  temporarily  unconscious.  In  other  cases  he  may  be  able 
to  walk,  in  a  dazed  condition,  to  the  nearest  field  dressing-station. 
He  at  once  finds  himself  to  be  totally  bhnd,  and  this  blindness  is 
often  accompanied  by  loss  of  smell,  taste,  and  hearing.     In  the 


Fig.  205. — Helicoicl  contraction  of  visual  fields  in  a  case  of  hysteria. 


early  days  of  such  shell-amblyopia  there  is  usually  intense  blepharo- 
spasm, so  that  voluntary  opening  of  the  lids  is  impossible  and  passive 
opening  is  excessively  difficult.  In  a  few  days  the  blepharospasm 
usually  passes  off,  but  the  patient  remains  for  a  time  blind  in  one 
or  both  eyes.  He  then  gradually  recovers  vision,  generally  passing 
through  a  stage  in  which  there  is  contraction  of  the  visual  fields, 
often  unequal  in  degree  in  the  two  eyes.  Ultimately  he  makes  a 
complete  recovery. 

Space  does  not  permit  us  to  discuss  the  other  pecuHarities  of 
hysterical  eye-affections  and  of  hysterical  loss  of  smell,  taste,  and 
hearing,  but  we  may  mention,  in  passing,  that  complete  bilateral 
loss  of  taste  is,  as  Hughlings  Jackson  pointed  out,  practically 
always  hysterical. 


400  NERVOUS    DISEASES 

Hysterical  Parcesthesia,  or  Perversion  of  Sensation. — In  some 
cases  of  hysteria  a  touch  on  one  limb  or  one  side  of  the  body  is 
felt  by  the  patient  at  the  corresponding  spot  on  the  opposite  side — 
allocheiria  (Obersteiner).  In  another  variety,  of  which  I  have  seen 
an  example,  a  touch  on  the  radial  border  of  the  Hmb  was  felt  on 
the  ulnar,  and  vice  versd.  Hafhalgesia  (Pitres)  is  the  term  used 
when  intense  pain  is  caused  by  touching  the  patient  with  certain 
substances,  such  as  metals,  which  normally  should  only  cause  a 
tactile  sensation. 

Parsesthesia)  of  the  special  senses  are  also  meb  with,  as,  for  ex- 
ample, in  monocular  diplopia  or  polyopia,  which  is  always  hysterical. 
Micropsia,  wheve  everything  looks  very  minute, and  macropsia,wh.eve 
surrounding  objects  seem  gigantic,  are  both  frequently  hysterical. 

Motor  Phenomena.— These  may  be  subdivided  into  irritative 
and  paralytic.  Amongst  the  irritative  phenomena,  the  most 
striking  are  the  so-called  hysterical  fits  or  paroxysms.  Hysterical 
fits  vary  enormously  in  type  and  in  severity,  from  a  simple  emo- 
tional outburst  of  uncontrollable  laughter  or  weeping,  accompanied 
perhaps  by  the  hysterical  "  globus  "  or  "  ball  in  the  throat,"  to  the 
most  prolonged,  dramatic  and  violent  muscular  movements,  together 
with  apparent  unconsciousness. 

One  variety  of  hysterical  fit  is  sometimes  mistaken  for  epilepsy, 
and  there  is  all  the  greater  habihty  to  make  this  mistake  since  the 
fit  is  generally  over  before  we  reach  the  patient,  and  we  are 
dependent  for  our  information  upon  the  accounts,  more  or  less 
accurate,  of  unskilled  witnesses.  But  if  the  physician  is  lucky 
enough  to  be  present  during  a  fit,  there  is  seldom  any  difficulty 
in  diagnosis.  Thus,  for  example,  the  patient  never  hurts  herself 
in  falling ;  there  is  no  stertorous  breathing ;  her  face  is  not  hvid, 
nor  does  she  bite  her  tongue  as  in  epilepsy  ;  she  may,  however,  bite 
her  lips  or  snap  at  the  fingers  of  the  bystanders.  She  never 
empties  the  bladder  or  rectum  during  the  fit ;  her  eyes  are 
usually  tightly  closed,  and  if  the  physician  tries  to  open  them, 
the  patient  resists  actively.  A  hysterical  fit  is  not  followed  by 
coma  and  hardly  ever  by  vomiting. 

But  we  must  remember  that  sometimes  we  have  hysterical  fits 
which  are  post-epileptic — i.e.  which  immediately  succeed  an  attack 
of  true  epilepsy.  The  antecedent  epileptic  fit  in  such  cases  is 
usually  of  the  "  petit-mal "  type,  consisting  perhaps  in  a  mere 
transient  pallor  of  the  face,  with  momentary  loss  of  consciousness, 


THE   NEUROSES  401 

and  then  passing  directly  into  a  hysterical  fit.  Therefore,  in  every 
case  it  is  important  to  inquire  very  carefully  as  to  the  precise 
mode  of  onset,  lest  we  overlook  a  case  of  combined  epilepsy  and 
hysteria. 

Charcot's  "  grande  [hysterie,"  with  its  initial  period  simulating 
epilepsy  and  its  subsequent  phases  of  contortions,  kicking,  and 
struggling  (clownism),  attitudes  fassionies  (opisthotonos,  cruci- 
fixion attitude,  &c.),  and  delirium,  often  with  hallucinations  of 
animals,  is  less  common  in  this  country  than  in  France,  but  once 
seen,  it  is  a  magnificent  performance  and  can  never  be  forgotten. 
It  is  totally  unhke  any  kind  of  epileptic  or  organic  fit,  and  its 
diagnosis  is  easy.  It  may  last  from  a  quarter  of  an  hour  to  several 
hours  at  a  time.  This  "  status  hystericus  "  is  commoner  than  the 
"  status  epilepticus,"  but  the  patient  has  no  subsequent  stupor 
such  as  that  which  succeeds  a  severe  epileptic  fit. 

Amongst  other  varieties  of  fits,  to  which  we  can  only  briefly 
refer,  we  may  mention  catalepsy,  in  which  the  patient  suddenly 
becomes  speechless,  motionless,  and  stiff.  Sometimes  she  is 
conscious  all  through  the  fit,  at  other  times  she  is  in  a  dreamy 
mental  state.  Meanwhile,  if  the  limbs  be  passively  moved  into 
any  posture,  however  fantastic,  they  remain  fixed  there  like  a 
doll's  limbs.  In  one  case  of  mine  the  patient,  a  woman  of  28, 
could  be  lifted  up  during  the  attack  by  the  head  and  heels  and 
laid  across  two  chairs  Hke  a  log. 

Hysterical  trance  may  come  on  spontaneously,  or  may  succeed 
a  hysterical  paroxysm.  It  is  a  condition  in  which  the  patient 
appears  as  if  in  a  deep  sleep  ;  but  the  muscles  are  seldom  com- 
pletely relaxed,  and  we  may  observe  shght  tremors  of  the  eyelids. 
In  more  severe  cases,  the  heart  and  respiration  may  become  so 
feeble  and  slow  that  the  condition  simulates  death.  Hysterical 
trance  may  last  hours,  days,  or  weeks  ;  and  several  cases  have 
been  authenticated  in  which  such  a  patient  has  been  buried  ahve, 
either  deliberately,  as  in  the  case  of  some  Indian  fakirs,  or  by 
accident  in  this  country.  Novehsts  know  this,  and  when  the 
heroine  is  thus  buried,  she  is  exhumed  in  the  last  chapter  by  the 
villain  for  the  sake  of  a  magnificent  diamond  ring  on  her  finger  ; 
whilst  her  finger  is  being  cut,  to  get  the  ring  off,  the  patient 
awakes. 

We  can  only  mention  other  varieties,  such  as  somnambulism 
and   double    consciousness,  this    latter,  when   in   extreme    degree, 

2  c 


402  NERVOUS    DISEASES 

being  a  condition  in  which  the  patient's  character  alternates 
between  normal  and  abnormal,  the  two  individuahties  being 
mutually  unconscious  of  each  other,  but  each  one,  as  its  turn 
comes,  takes  up  the  thread  where  it  had   previously  left  off. 

A  minor  degree  of  double  consciousness  can  be  demonstrated, 
by  a  simple  experiment,  in  many  cases  of  hysteria  in  which 
there  happens  to  be  hysterical  ansesthesia  of  the  upper  limb.  If 
in  such  a  case  we  screen  the  anaesthetic  limb  from  the  patient's 
view,  she  does  not  feel  pin-pricks  or  touches  on  the  limb,  nor  does 
she  recognise  familiar  objects  when  placed  in  the  hand.  But  if  a 
pencil  be  placed  in  the  "  screened  "  hand,  it  is  grasped  in  a  position 
suitable  for  writing,  and  if  we  now  trace  a  letter  or  a  word  on  the 
back  of  the  anaesthetic  hand  (the  patient's  attention  meanwhile 
being  diverted  by  another  observer)  this  letter  or  word  is  repro- 
duced in  writing,  entirely  unknown  to  the  patient's  consciousness. 
Analogous  sub-conscious  phenomena  can  be  demonstrated  in  many 
apparently  normal  people  by  means  of  a  small  wheeled  platform 
or  "  planchette  "  carrying  a  pencil. 

We  also  meet  with  a  hysterical  type  of  anibidatory  automatism 
where  the  patient  (more  often  a  man  than  a  woman)  has  attacks 
in  which,  without  adequate  motive,  he  has  a  sudden  and  irresistible 
impulse  to  wander  from  home.  He  makes  a  long  journey,  some- 
times undergoing  great  hardships  en  route.  Finally,  days,  weeks, 
or  even  months  afterwards,  he  suddenly  wakes  up  in  some  strange 
town  or  country,  entirely  unaware  of  how  he  got  there.  For 
example,  I  have  known  of  a  boy  who  disappeared  from  school  in 
this  way,  of  a  young  officer  who  deserted  from  his  regiment,  and 
of  a  business  man  who  left  his  wife  and  family,  in  all  these  cases 
without  any  adequate  cause.  These  cases  are  closely  related  to 
the  somnambulistic  stage  of  the  hypnotic  trance,  and  if  such  a 
patient  be  hypnotised  he  becomes  able  to  give  a  complete  account 
of  his  wanderings  from  the  moment  of  his  disappearance  to  the 
time  when  he  woke  up  and  "  found  himself."  The  diagnosis 
between  hysterical  and  post-epileptic  ambulatory  automatism,  to 
which  we  have  already  referred  (p.  78),  is  not  always  easy.  We 
should  carefully  inquire  for  evidences  of  epilepsy,  major  or  minor, 
we  should  look  for  the  presence  of  hysterical  stigmata  (though 
even  in  hysterical  cases  stigmata  may  be  absent),  whilst  the  recon- 
struction of  the  "  lost  "  period  of  time  when  in  the  hypnotic  trance 
is  highly  suggestive  of  its  hysterical  origin. 


THE    NEUROSES  403 

Various  localised  motor  disturbances  also  occur  in  hysteria  and 
psycliasthenia.  Such,  for  example,  is  the  large  group  of  "tics"  and 
"habit  spasms"  which  we  have  already  studied  (p.  100).  A  true  tic 
is  essentially  and  primarily  a  psycho-motor  act,  either  an  emotional 
expression  or  a  movement  which  has  become  a  habit.  Of  these  tics, 
the  commonest  are  grimaces,  jerkings  of  the  head,  trunk,  or  limbs, 
and  tremors  of  various  parts,  rapid  or  slow.  Thus,  for  example,  a 
lady's  maid,  aged  46,  had  tonic  spasm  of  the  orbicularis  oculi  on 
both  sides  (blepharospasm),  and  could  open  her  eyes  only  by 
opening  the  mouth  as  well.  Another  girl,  set.  19,  had  a  clonic  or 
jerking  paroxysmal  blepharospasm,  associated  with  "  humping  up  " 
of  one  foot.  Another  girl  of  19  had  rapid  "  twiddUng  "  movements 
of  the  left  thumb  and  fingers,  with  pronation-supination  movements 
of  the  forearm  and  a  pseudo-clonus  of  the  left  ankle.  Another 
girl,  aged  20,  who  previously  had  suffered  long  from  recurrent 
vulval  abscesses,  had  attacks  of  rapid  antero-posterior  movements 
of  the  pelvis.  Another  patient  had  rapid  violent  flexion-extension 
movements  of  the  left  elbow  whenever  a  thunderstorm  occurred, 
the  hand  meanwhile  dangling  loosely  at  the  wrist.  Such  cases 
of  localised  motor  disturbances  might  be  multiplied  almost  ad 
infinitum. 

Hysterical  Paralysis  may  be  either  flaccid  in  type,  simulating 
a  lower  motor  neurone  lesion,  or  spastic,  simulating  an  upper  motor 
neurone  lesion.  It  may  affect  any  of  the  voluntary  muscles  ;  but, 
unlike  paralysis  due  to  organic  lesions,  it  never  attacks  a  single 
muscle  nor  the  muscles  supplied  by  a  single  nerve,  nor  are  the 
electrical  reactions  of  degeneration  ever  present.  A  further  point 
about  hysterical  paralysis  is  that,  though  it  may  roughly  resemble 
the  posture  of  an  organic  paralysis,  it  never  does  so  with  accuracy  ; 
there  is  always  some  point  of  difference  to  be  detected.  The  reason 
for  this  we  have  already  discussed  (p.  290). 

Let  us  study  examples  of  hysterical  monoplegia,  of  paraplegia, 
and  of  hemiplegia. 

Fig.  206  is  that  of  a  nurse,  aged  32,  with  hysterical  monoplegia 
of  the  right  arm  of  eight  months'  duration,  in  whom  there  was  extreme 
muscular  wasting  and  claw-hand.  The  paralysis  came  on  after  a 
strain  of  the  shoulder  in  lifting  a  heavy  patient,  and  somewhat  re- 
sembled a  lesion  of  the  brachial  plexus.  But  we  observed  that  the 
trapezius  was  paralysed,  and  that  the  whole  scapula  was  displaced 
downwards— unlike  an  organic  brachial-plexus  case,  in  which  the  arm 


404 


NERVOUS    DISEASES 


would  be  displaced  downwards  at  the  shoulder-joint.  Moreover,  the 
electrical  reactions  were  normal  in  the  wasted  muscles,  and  there  was 
a  "  glove  "  of  anaesthesia,  unlike  the  "  root  "  anaesthesia  of  an  organic 
case.  The  patient  was  treated  for  several  weeks  by  battery  and  mas- 
sage, without  effect  at  first,  but  the  result  proved  our  diagnosis  to  be 
correct,  for  at  a  religious  meeting  she  was  suddenly  cured. 

Fig.  207  shows  a  case  of  hysterical  monoplegia  of  the  left  upper 
limb  in  a  young  man  of  21  who  was  screwing  on  the  bulb  of  an  electric 
lamp  when  the  current  became  short-circuited,  the  bulb  burst,  and  he 
had  a  sudden  electric  shock  through  the  left  hand.     When  examined 


Fig.  206. — Hysterical  monoplegia  of  right  upper  limb,  accompanied  by 
muscular  atrophy,  but  without  changes  in  electrical  reactions. 


nine  months  after  this  accident,  there  was  total  flaccid  paralysis  and 
complete  anaesthesia  of  the  left  upper  limb,  which  dangled  helplessly 
in  a  flail-like  fashion.  The  latissimus  dorsi,  however,  although  paralysed 
for  voluntary  movements,  contracted  briskly  when  coughing.  All  the 
muscles  of  the  limb  reacted  briskly  to  faradism. 

In  spite  of  assiduous  suggestive  treatment  of  various  kinds  in  hos- 
pital, including  powerful  electrical  stimulation,  the  application  of 
cutaneous  irritants,  and  attempts  at  hypnotic  suggestion,  no  improve- 
ment occurred.  Eleven  months  after  the  onset  of  his  symptoms, 
before  discharging  the  patient,  it  was  decided  to  trj^  the  effect  of  a 
general  anaesthetic  in  the  hope  of  loosening  his  obsession  during  the 
stage  of  excitement.     The  result  was  dramatic.     Within  a  few  seconds 


THE    NEUROSES 


405 


after  commencing  the  inhalation  of  ether  and  nitrous  oxide  freely 
mixed  with  air,  the  patient  began  to  move  the  paralysed  limb,  and  in 
a  short  time  he  was  fighting  violently  with  it.  The  anaesthetic  was 
then  discontinued,  and  the  patient  passed  into  a  hypnotic  state,  during 
which  voluntary  movements  of  the  previously  paralysed  limb  were 
normally  executed  in  obedience  to  verbal  commands,  accompanied 
by  occasional  painful  stimuli,  such  as  twisting  the  ear,  pricking  the 
previously  anaesthetic  limb,  &c.     It  was  then  suggested  to  liim  that 


Fig.  207. 


all  his  motor  and  sensory  disability  should  disappear,  and  as  the 
efiects  of  the  ether  passed  off  this  was  found  to  be  actually 
the  case.  Ever  after  the  foregoing  seance  he  remained  able  to 
move  his  limb  normallv,  the  anaesthesia  also  remaining  absent.  (See 
Fig.  208.) 

Figs.  197  and  197a  are  from  a  case  of  hysterical  flaccid  paraplegia 
of  fourteen  years'  duration  in  a  woman  of  37,  which  at  first  sight 
might  be  mistaken  for  a  cord-lesion  with  muscular  atrophy  and  anaes- 
thesia. But  the  anassthesia  was  of  the  "  stocking  "  type,  the  reflexes, 
deep  and  superficial,  and  the  electrical  reactions  were  normal,  the 


406 


NERVOUS    DISEASES 


sphincters  were  unaffected,  and  there  were  no  bed-sores  ;  and  the 
result  of  six  weeks'  isolation  and  massage  was  to  restore  the  power  of 
walking  (Fig.  198). 

In  some  cases  of  hemiplegia  the  posture  is  sufficient  to  diagnose 
hysteria.  For  example,  in  the  patient  shown  in  Figs.  130  and  131 
(p.  288),  instead  of  the  ordinary  posture  of  an  organic  case,  with  the 
upper  extremity  flexed  and  pronated,  the  lower  extremity  flexed  at 
the  hip,  extended  at  the  knee  and  ankle,  and  slightly  inverted,  there 


Fig.  208. 


was  a  curious  posture  of  the  hand  and  foot  unlike  that  of  organic 
disease.  Moreover,  her  face  entirely  escaped,  in  spite  of  the  severe 
paralysis  of  the  arm  and  leg  ;  and  she  had  hemi -anaesthesia  and 
loss  of  special  senses  down  one  side,  a  combination  which  never 
occurs  in  organic  hemiplegia. 

The  face  and  tongue  are  rarely  affected  in  hysterical  hemi- 
plegia. But  in  certain  cases  we  may  find  instead  of  weakness, 
spasm  of  the  face  and  tongue  on  the  affected  side,  when  the  patient 
shows  the  teeth  or  protrudes  the  tongue.     This  hysterical  glosso- 


THE    NEUROSES 


407 


labial  hemispasm  is  rare,  but  Figs.  209  and  133  (p.  289)  are  good 
examples  of  the  condition. 

We  may  also  refer  to  "  Lasegae's  symptom "  (Nothnagers 
"Seelenldhmung^^)  in  which  a  patient  with  an  anaesthetic  limb  cannot 
move  it  when  the  eyes  are  closed,  but  is  able  to  move  it  when  she 
opens  her  eyes  and  looks  at  it.  Another  feature  worthy  of  mention 
is  hysterical  pseudo -ptosis.     In  organic  ptosis  due  to  lesion  of  the 


Fig.  209. — Glosso-labial  hemi-spasm.     Left-sided. 


third  cranial  nerve,  there  is  always  a  compensatory  over-action  of 
the  frontalis  muscle.  But  in  hysterical  pseudo-ptosis  this  is  absent, 
and  the  condition  is  really  due,  not  to  paralysis  of  the  levator 
palpebrse,  but  to  spasm  of  the  orbicularis  ocuU  (see  Fig.  67,  p.  146). 

Before  leaving  the  motor  phenomena  of  hysteria,  it  may  be 
well  to  refer  to  the  gaits  of  hysterical  and  psychasthenic  patients, 
which  are  sometimes  most  peculiar. 

Astasia-ahasia  is  a  hysterical  condition  in  which,  although  the 


408 


NERVOUS    DISEASES 


patient  can  move  his  legs  normally  when  lying  or  sitting,  he 
collapses  at  once  when  he  tries  to  stand  or  walk.  Children  are 
more  often  affected  than  adults.  A  httle  girl,  aged  10,  had  this 
symptom  for  twelve  months  (see  Fig.  210),  but  was  cured  in  a 


Fig.  210. 


Fig.  210a. 


couple  of  minutes  by  an  application  of  high-frequency  sparks  in  a 
darkened  room,  accompanied  by  the  suggestion  that  she  could 
now  walk  (Fig.  210a).  One  patient,  a  doctor  aged  55,  used  to 
flourish  his  left  leg  [in  the  air  and  bring  it  down  with  a  stamp 
like  that  of  a  unilateral  locomotor  ataxia.  This  phenomenon,  an 
ambulatory  tic,  was  so  dramatic  that  he  had  to  carry  a  stick  to 


THE    NEUROSES 


409 


beat  off  tlie  crowds  of  little  boys  who  studied  his  gait  in  the 
streets.  Another  patient  was  a  worthy  married  lady  who  every 
now  and  then,  when  walking,  sat  down  suddenly  on  the  ground, 
rolled  backwards  and  spread  out  her  lower  limbs  like  the 
letter  V. 

Perhaps  the  commonest  hysterical  gait  is  a  dragging  gait,  in 
which  the  patient  trails  the  limb  helplessly  along,  often  scraping 
the  inner  border,  or  even  the  dorsum  of  the  foot,  on  the  ground 
(see  Fig.  141,  p.  296),  unlike 
organic  hemii)lcgia  in  which  the 
outer  side  of  the  sole  is  dragged . 

Some  authorities  state  that 
muscular  atrophy  does  not  occur 
in  a  hysterical  limb.  But  this 
is  not  accurate,  for  in  certain 
rare  cases,  one  of  which  is  shown 
in  Fig.  206,  we  may  meet  with 
profound  atrophy.  But  this 
atrophy  is  due  to  disuse  and  is 
not  associated  with  the  electrical 
reactions  of  degeneration. 

Contractures  of  the  most  pro- 
nounced type  may  be  met  with 
in  hysterical  paralysis.  But  here, 
again,  they  always  differ  in  some 
respect  from  those  of  organic 
cases.  Fig.  211  is  the  photo- 
graph of  a  soldier,  aged  32,  whose 
horse  rolled  on  him  at  the  Tugela, 
and  who  afterwards  developed  a 
stiff  left  arm,  flexed  at  the  elbow  and  wrist,  and  with  the  thumb 
and  index  finger  held  stifily  parallel. 

A  study  of  the  reflexes  is  of  great  diagnostic  importance  in 
every  case  of  hysteria.  The  deep  reflexes  are  normal  or  exag- 
gerated, and  sometimes  accompanied  by  a  feeling  of  acute  inde- 
scribable discomfort.  In  pure  hysteria  they  are  never  lost,  although 
sometimes  they  may  be  "  concealed "  by  the  presence  of  mus- 
cular spasm.  True  ankle-clonus  does  not  occur,  but  a  pseudo- 
ankle-clonus  is  often  met  with.  In  a  girl  of  19,  the  subject 
of  thread-worms  and  pruritus  ani,  this  pseudo-ankle-clonus  used 


Fig.  211. — Hysterical  contracture  of 
the  left  hand  and  elbow,  following 
an  injury  to  the  elbow. 


410  NERVOUS    DISEASES 

to  come  on  spontaneously  when  sitting  or  standing  at  ease.  One 
can  often  distinguish  it  from  a  true  organic  clonus  by  the  pecuHar 
upward  start  of  the  foot  before  it  sets  of?  on  its  first  downward 
push.     Further,  pseudo-clonus  is,  as  a  rule,  poorly  sustained. 

The  superficial  reflexes  are  often  diminished,  especially  on  the 
anaesthetic  side.  The  pharyngeal  reflex  is  frequently  abolished. 
The  plantar  reflex  in  hysteria,  if  present,  is  always  of  the  normal 
flexor  type,  never  of  the  extensor  or  Babinski  type.  A  persistent 
extensor  plantar  reflex  only  occurs  in  cases  of  disease  of  the  pyra- 
midal tracts,  and  in  infants  who  have  not  learned  to  walk  and  in 
whom  the  pyramidal  tracts  are  not  yet  myelinated. 

The  pupil-reflex  to  light  is  never  lost  in  pure  hysteria, 
though  in  rare  cases  it  may  be  "  concealed  "  by  the  presence  of 
pupillary  spasm.  I  remember  one  case  of  fixed  dilated  pupils 
in  a  hysterical  woman,  but  this  was  due  to  the  taking  of 
belladonna  by  the  patient. 

Another  useful  test  is  afforded  by  Leri's  forearm  sign.^  This 
consists  in  an  involuntary  flexion  movement  of  the  elbow  when 
the  observer  passively  flexes  the  fingers  and  wrist.  In  organic 
hemiplegia  this  forearm  sign  is  lost,  whereas  in  hysterical  paralysis 
it  remains  positive. 

As  to  the  bladder  and  rectum,  although  we  may  have  frequency 
of  micturition  in  hysteria,  we  never  have  true  incontinence.  Re- 
tention of  urine,  on  the  other  hand,  is  a  fairly  common  symptom. 
It  once  broke  out  as  an  acute  epidemic  in  a  school  for  young  ladies 
and  continued  until  the  doctor  judiciously  handed  over  the  duty 
of  catheterisation  to  a  female  nurse  of  mature  years.  The  symptom 
at  once  subsided  in  a  gratifying  manner. 

Visceral  and  Vaso-motor  Phenomena. — It  is  important  to 
remember  that  hysteria  affects  the  vegetative  nervous  system 
as  well  as  the  cerebro-spinal.  Let  us  refer  very  briefly  to  some 
of  the  visceral  and  vascular  phenomena. 

We  may  meet  with  abnormal  slowness  of  the  heart,  or  we  may 
observe  abnormal  rapidity  with  palpitation,  chiefly  paroxysmal, 
constituting  a  variety  of  pseudo-angina,  especially  in  hysterical 
or  neurasthenic  young  mothers  who  have  been  lactating  too  long. 
This  condition  is  easily  distinguished  from  true  angina  by  the 
absence  of  signs  of  organic  cardio -vascular  disease. 

In  the  digestive  system  we  meet  with  curious  hysterical  pheno- 

^  Revue  neurologique,  March  15,  1913. 


THE    NEUROSES  411 

mena.  Aerophagy,  or  swallowing  of  air,  is  achieved  chiefly  by 
gulping  movements  of  the  pharynx.  I  remember  a  little  school- 
boy who  could  swallow  air  and  distend  his  abdomen  till  his 
waistcoat  could  not  be  buttoned.  We  are  all  famihar  with 
hysterical  dysphagia  or  spasm  of  the  oesophagus,  with  its  sudden 
intermissions  and  the  difficulty  experienced  equally  with  liqmds 
and  with  solids,  in  which  nevertheless  a  large  stomach-tube  can  be 
easily  passed.  The  hysterical  "  globus  "  or  "  ball  in  the  throat," 
which  the  patient  tries  to  swallow,  is  an  emotional  phenomenon 
often  met  with  at  the  onset  of  a  hysterical  paroxysm.  Hysterical 
vomiting  has  always  to  be  excluded  in  gastric  disorders  of  young 
women.  It  is  often  associated  with  anorexia  nervosa,  where  the 
patient  will  take  hardly  any  food.  "  Fasting  girls,"  of  whom  we 
now  and  then  read  in  the  newspapers,  are  generally  examples  of 
this  kind  of  hysteria.  They  may  become  extraordinarily  emaciated, 
but  even  they  do  take  a  httle  food  now  and  then. 

Rhythmic  movements  of  the  stomach  or  intestine  accompanied 
by  curious  rumbling  noises  are  sometimes  met  with.  They  are 
usually  vagotonic  neuroses.  The  commonest  variety  is  the  in- 
testinal, and  at  dinner-parties  one  sometimes  hears  these  noises 
in  nervous  young  servant-maids  waiting  at  table.  Much  less 
frequently  we  hear  violent  gastric  borborygmi.  One  young  girl 
whom  I  saw  had  constant,  noisy  to-and-fro  gurghng  in  the  upper 
part  of  the  abdomen,  like  a  steam-pump,  and  on  palpating 
the  abdomen  the  stomach  could  be  felt  rhythmically  contracting 
and  relaxing,  blowing  and  sucking  air  backwards  and  forwards. 
This  phenomenon  was  so  starthng  to  strangers  that  the  unfor- 
tunate girl  had  to  retire  to  her  own  room  if  friends  came  to  call 
on  the  family.  '  Somewhat  similar  abdominal  noises  in  another 
hysterical  patient,  a  lad  of  19,  were  apparently  produced  by 
spasmodic  contractions  of  the  diaphragm,  for  they  ceased  when 
he  drew  a  deep  breath  and  held  it. 

The  artiste  who  earned  an  honest  Uving  at  a  Parisian  music 
hall  by  making  musical  noises  with  his  anus  was  probably  another 
example  of  visceral  hysteria. 

We  must  also  bear  in  mind  the  pseudo-pregnancies  which  now 
and  then  occur,  in  which  spurious  enlargement  of  the  abdomen 
sometimes  goes  on  to  a  spurious  labour.  Then  "  parturiunt  monies, 
nascitur  ridiculus  mus  " — all  that  is  produced  being,  at  the  most, 
a  small  uterine  cast.     Phantom  abdominal  tumours  can  best  be 


412  NERVOUS    DISEASES 

differentiated  from  genuine  ovarian  or  uterine  enlargements  by 
giving  a  general  ansesthetic,  when  the  abdomen  at  once  collapses. 

It  is  sometimes  more  difficult  to  diagnose  pseudo-appendicitis. 
Thus  one  patient  whom  I  saw,  aged  33,  had  had  her  abdomen 
opened  twice  in  different  London  hospitals  for  supposed  appendicitis, 
the  symptoms  being  those  of  recurrent  pain  and  tenderness  in  the 
right  iliac  fossa,  with  constipation  and  vomiting.  But  she  had 
also  right-sided  hemi-anaesthesia,  with  loss  of  special  senses  all  down 
that  side.  We  were  thus  led  to  suspect  the  hysterical  nature  of 
the  abdominal  symptoms,  and  accordingly  her  next  attack  was 
cured  by  sal  volatile,  without  laparotomy,  and  she  has  had  none 
since. 

Hysterical  diarrhoea  sometimes  occurs,  as  in  the  case  of  a  public 
speaker  who  was  often  attacked  in  this  awkward  way  just  when 
his  turn  arrived  to  address  the  audience.  Cases  like  this  are  tran- 
sient and  unaccompanied  by  fever,  anorexia,  or  general  malaise, 
as  in  diarrhoea  from  organic  causes. 

Spontaneous  hsemorrhages  are  very  rare  in  hysteria,  and  no 
hsemorrhage  should  ever  be  diagnosed  as  hysterical  unless  all  other 
causes  can  be  excluded.  But  a  certain  number  of  cases  of  pseudo- 
hsemoptysis  and  pseudo-hsematemesis  occur.  In  one  girl  whom  I 
watched,  the  phenomenon  seemed  to  be  produced  by  sucking  of 
the  gums  ;  in  another  it  was  apparently  the  result  of  pharyngeal 
suction.  In  both  cases,  physicians  of  wide  experience  who  saw 
the  case  in  consultation  failed  to  discover  any  organic  cause  in  the 
chest  or  abdomen. 

Sometimes  a  limb  affected  by  hysterical  paralysis  or  anaesthesia 
may  show  abnormal  vasomotor  spasm,  so  that  if  pricked  or  cut  it 
bleeds  less  freely  than  normal.  A  soldier  at  the  battle  of  Ypres 
was  presenting  his  rifle  to  fire,  when  it  was  struck  by  a  shell  with- 
out wounding  the  man.  He  at  once  developed  hysterical  paralysis 
of  the  upper  and  lower  Hmbs,  of  flaccid  type,  and  without  sphincter 
trouble,  lasting  for  several  weeks,  and  accompanied  by  coldness 
and  cyanosis  of  the  hands  and  feet,  the  radial  pulses  being  im- 
palpable.    All  the  symptoms  gradually  disappeared. 

Secretory  phenomena  also  occur,  though  rarely,  as  for  example 
in  blood-stained  tears  or  blood-stained  sweat  or  mammary  secre- 
tion, which  may  be  unilateral.  Polyuria  often  occurs  after  a 
hysterical  fit,  whereas  hysterical  anuria  or  suppression  of  urine  is 
extremely  uncommon. 


THE    NEUROSES  413 

Certain  skin  affections  may  occur  in  hysterical  patients.  Cuta- 
neous haemorrhages  are  rare,  if  we  exclude  cases  of  voluntary 
traumatism.  Bed-sores  do  not  occur.  The  gangrenous  patches 
described  as  hysterical  gangrene  are  always  self-inflicted,  by  means 
of  caustics  or  other  methods  (see  Fig.  141,  p.  296).  Hysterical 
blue  oedema  sometimes  occurs,  especially  in  contractured  limbs, 
but  is  generally  a  fraudulent  phenomenon,  self-produced  by  the 
patient,  who  ties  a  constricting  band  around  the  limb.  When 
occurring  spontaneously,  it  usually  affects  the  skin  over  a  joint 
and  produces  a  degree  of  cyanosis  and  swelhng,  but  this  swelling 
does  not  pit  on  pressure.  Hysterical  oedema  may  last  for  weeks 
or  months.  It  generally  disappears  suddenly.  Thus  in  a  case 
recorded  by  Raymond,  it  suddenly  cleared  up  when  the  patient 
had  the  glad  stimulus  of  an  unexpected  legacy.  Dermographism 
is  commoner  in  hysterics  than  in  normal  people.  Fig.  212  is  an 
excellent  example  in  a  girl  with  hysterical  tremor  of  the  legs,  in 
whom,  when  the  skin  was  stroked  with  the  finger-nail,  a  white 
raised  wheal  appeared  and  remained  for  an  hour  or  more.  This 
"  factitious  urticaria "  or  "  urticaria  scripta,"  unlike  ordinary 
urticaria,  does  not  itch. 

Hysterical  cough  is  very  common ;  it  is  usually  loud  and 
hacking,  going  on  all  day  and  ceasing  during  sleep.  It  is  not 
accompanied  by  expectoration,  and  is  commonest  in  young 
hysterics.  We  may  have  other  peculiar  modifications  of  respira- 
tion. Thus  in  a  girl  of  24  who  had  hysterical  fits,  expiration 
was  a  curious  grunting  noise  of  a  bigeminal  type — two  grunts 
between  each  inspiration.  We  also  meet  with  paroxysmal  rapid 
breathing,  sneezing,  hiccup,  and  yawning.  One  girl,  aged  10,  the 
subject  of  hysterical  hemi-ansesthesia,  yawned  persistently  for  three 
weeks  during  her  waking  hours.  She  then  stopped  and  had  an 
attack  of  hysterical  mutism  lasting  for  two  months. 

When  hysteria  occurs  in  childhood  it  is  often  mono -sympto- 
matic and  the  ordinary  hysterical  stigmata  are  frequently  absent. 
Girls  are  much  more  frequently  affected  than  boys,  even  before 
the  age  of  puberty.  Perhaps  the  commonest  symptoms  of  hysteria 
in  childhood  are  astasia-abasia  and  hysterical  aphonia.  The  various 
forms  of  habit-spasm  are  common  in  young  psychasthenics. 

The  diagnosis  between  hysteria  and  organic  disease  is  some- 
times easy ;  in  other  cases  it  is  a  matter  of  extreme  difl&culty. 
In  doubtful  cases  special  attention  should  be  paid  not  only  to  the 


414 


NERVOUS    DISEASES 


psychical  symptoms  but  to  the  special  senses,  to  the  condition  of 
the  optic  discs,  to  the  type  of  anaesthesia  which  may  be  present, 
to  the  posture  of  the  limbs  in  cases  with  motor  paralysis,  and  to 


Fig.  212. — Case  of  dermographism  in  a  hysterical  young  woman. 

the  condition  of  the  reflex;es,  especially  the  plantar  reflex  and  the 
bladder  functions.  Lastly,  we  should  never  forget  that  hysteria 
and  organic  disease  may  coexist  in  the  same  case. 


CHAPTER   XXII 

ELECTRO-DIAGNOSIS   AND   ELECTiiO-PHOGNOSIS 

It  is  not  necessary  to  enter  into  a  full  discussion  of  the  various 
physiological  phenomena  produced  by  electrical  stimulation  of 
difierent  tissues,  still  less  to  discuss  the  nature  of  electricity  itself 
or  the  rationale  of  its  effects.  It  will  suffice  here  to  recall  a 
few  of  the  more  practical  points  in  the  physiology  of  electrical 
stimulation. 

Chnically,  electrical  stimulation  is  of  value  chiefly  in  the 
examination  of  muscles  and  of  motor  nerves.  Electrical  examina- 
tion of  sensory  functions  is  of  but  httle  practical  importance, 
except  perhaps  when  mapping  out  areas  of  loss  of  taste,  when 
a  mild  galvanic  current  is  an  excellent  gustatory  stimulus. 

For  diagnostic  purposes  the  three  most  important  forms  of 
electricity  are  the  faradic,  interrupted,  or  induced  current,  the 
galvanic  or  continuous  current,  and  the  vibrant  electricity,  which 
is  the  result  of  discharging  a  powerful  induced  current  through 
a  Crookes'  vacuum-tube,  producing  the  well-known  X-rays.  The 
application  of  this  latter — so-called  skiagraphy,  though  of  great 
practical  importance,  does  not  specially  concern  the  neurologist. 
We  have  to  consider  more  particularly  the  faradic,  the  galvanic, 
and  the  condenser  currents. 

To  produce  the  galvanic  current,  we  employ  a  galvanic  battery 
(preferably  a  dry-cell  battery,  which  can  be  carried  about  without 
spilhng)  and  this  battery  must  have  sufficient  electro-motive  force 
or  voltage  to  overcome  the  resistance  of  the  skin,  which  is  a  bad 
conductor,  and  to  stimulate  the  muscles  and  nerves  underneath.  In 
cities  where  there  is  an  electric  hght  system  run  by  the  continuous 
current,  we  can  utiHse  this  current  to  charge  an  accumulator  which 
can  be  carried  about,  or  we  may  use  the  current  direct  from  the 
main,  provided  we  are  careful  to  reduce  the  voltage  sufficiently. 
This  is  accomplished  by  means  of  shunts,  resistances,  or  rheostats. 

Faradic,  or  induced  electricity,  is  obtained  by  induction.    In 

415 


416 


NERVOUS    DISEASES 


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ELECTRO-DIAGNOSIS 


417 


a  faradic  macliine  there  are  two  coils  of  wire,  concentrically  placed 
— ^the  primary  coil  within  the  secondary.  When  a  galvanic 
current  passes  along  the  primary  coil,  there  is  produced,  at  the 
moment  of  closure  and  again  at  the  moment  of  opening  of  the 
primary  current,  an  instantaneous  faradic  shock  in  the  secondary 
coil,  no  shock  occurring  during  the  period  of  flow  of  the  primary 
current,  so  long  as  its  strength  remains  constant.  Within  the 
primary  coil  there  is  usually  a  bundle  of  soft  iron  wire,  which 
becomes  converted  into  a  magnet  when  the  galvanic  stream  flows 
round  the  primary  coil.     Now  a  magnet  pushed  within  a  coil  pro- 


M.  rectus  abdo- 
minis {Abdo- 
minal intercostal 
nerves) 


M.  serrat.  magn. 
M.  latissimus 
dor.si. 

M.  obliquus 
abdom.  externus 

(Abdominal 
intercostal  nerves) 

M.  transversus 
abdominis. 


Fig.  214.— Motor  Points  of  Abdominal  Wall.     (Erb.) 


duces  an  instantaneous  faradic  or  induced  shock  in  that  coil ;  so  that 
as  the  soft  iron  is  alternately  magnetised  and  then  de-magnetised 
by  the  primary  coil,  we  have  the  effect  of  the  magnet  superadded 
to  that  of  the  primary  coil.  We  can  vary  the  strength  of  the 
faradic  shocks  in  the  secondary  coil  in  several  ways,  by  puUing 
the  iron  bundle  in  or  out,  or  by  sUding  a  cyhndrical  brass  shield 
between  the  primary  and  secondary  coils  (the  effect  on  the 
secondary  coil  being  greatest  when  no  shield  is  interposed),  or 
lastly,  by  having  the  secondary  coil  on  a  sUding  sledge,  so  that  we 
can  pull  the  two  coils  apart.  This  last  is  the  best  and  most  deli- 
cate way  of  varying  the  intensity  of  the  faradic  shocks  in  the 
secondary  coil. 

We  apply  the  electrical  current  to  muscles  and  nerves  by  means 

2  D 


418 


NERVOUS    DISEASES 


of  metal  electrodes  of  various  sizes,  some  flat  and  disc-like,  others 
with  rounded  bulbous  ends.  The  metal  surface  of  the  electrode 
should  be  covered  with  chamois-leather.  The  electrode  is 
screwed  on  to  a  holder,  which  must  have  a  contact-key  whereby 
we  can  interrupt  the  current  at  will.  The  chamois-leather  should 
be  soaked  before  use,  and  the  skin  should  also  be  well  moistened, 
in  warm  water  to  which  a  little  salt  has  been  added,  to  render  it  a 


M.   deltoideus  (pos 
terior  half) 


Musculo- spiral  nerve 
M.  bracial.  antic. 

M.  supinator  long. 

M.  radial,  ext.  long. 

M.  radial  ext.  brev. 

M.  extensor  digit.  I 

communis        \ 

M.  extensor  indicia 
M.  abductor  pollic.  long. 
M.  extensor  pollic  brev. 


M.  inteross.  dorsal 
I.  et  II. 


M.  triceps  (long  head) 


M.  triceps  (outer  head) 


M.  extensor  carpi  ulnari 
M.  supinator  brevis 

M.  extensor  digiti  minimi 
M.  extensor  indicis 

::^  l-M.  estens.  poll.  long. 


M.  abduct,  digit,  min. 

M.  inteross.  dorsal. 

III.  et  IV. 


Fig.  215.— Motor  Points  of  Upper  Limb.     (Erb.) 


better   conductor.     The  salt,   however,  spoils  the  leather,   which 
must,  in  consequence,  be  frequently  renewed. 

We  should  have  a  galvanometer  in  the  circuit  of  the  galvanic 
current,  so  as  to  measure  the  strength  of  current  which  pene- 
trates the  tissues.  There  should  also  be  a  commutator  or  shding 
switch,  whereby  we  can  reverse  the  direction  of  the  current. 
The  galvanic  battery  should  be  fitted  with  a  collector  whereby 
we  can  switch  on  the  different  cells,  one  by  one,  gradually  in- 
creasing the  strength  of  the  current. 


ELECTRO-DIAGNOSIS 


419 


In  testing  the  electrical  reactions  of  muscles,  one  electrode 
should  be  placed  on  the  spot  we  desire  to  stimulate,  whilst  the 
other  is  placed  on  some  far-distant  "  indifferent "  spot,  where  any 
muscular  contractions  that  may  occur  will  not  interfere  with  the 
part  we  are  observing.     Thus  the  indifferent  pole  may  be  placed 


M.  triceps  (long  head) 

M.  triceps  (inner  head) 
Ulnar  nerve  -j 


M.  flexor  carpi  ulnars. 

M.  flex,  digitor.  communi 
profund. 


M.  flex,  digitor.  sublim. 
(digitill.  etIII.) 
M.  flex,  digit,  subl.  (digit, 
indicia  et  minimi) 

Ulnar  nerve 

M.  palmari.s  brev. 

M.  abductor  digiti  min. 

M.  flexor  digit,  m  n, 

M.  opponens  digit,  min. 

Mm.  lumbrieales  < 


M.  deltoideus 
(anterior  half) 


Musculocutaneous 

nirve 
M.  biceps 
bracliii 

M.  brach. 
amicus 


Median  -nerve 
M.  supinator  longns 

M.  pronator  teres 
M.  flex,  carpi  radialis 


M.  flex,  digitor.  sublim. 

M.  flex.  poUicis  longus 
Median  nerve 

M.  abductor  pollic.  brev. 
M.  opponens  pollicis 

M.  flex.  poll.  brev. 

M  adductor  pollic. 


Fl  G.  216.  —Motor  Points  of  Upper  Limb.     (Erb.) 


on  the  back  of  the  neck,  or  on  the  front  of  the  abdomen,  or  the 
patient  may  sit  upon  it,  or  he  may  hold  it  in  the  opposite  hand. 
We  then  fix  our  attention  on  the  other  pole  which  we  are  watching. 
To  stimulate  isolated  nerves  or  muscles,  either  the  electrode  should 
be  a  small  one,  or  we  may  employ  the  edge  of  a  disc  electrode. 

The  patient  must  be  placed  in  a  good  hght,  so  that  we  can 
see  the  slightest  movement  of  the  muscle  we  are  examining.  Some- 
times by  placing  our  finger  on  the  tendon  of  the  muscle,  we  can 


420 


NERVOUS    DISEASES 


feel  a  contraction  too  faint  to  be  visible.  The  patient  should  be 
made  to  relax  all  the  muscles  of  the  regie n  which  is  under 
examination.  Before  applying  the  electrodes  to  the  patient,  we 
should  make  it  an  invariable  rule  to  test  the  strength  of  the  current 
on  our  own  skin,  to  avoid  startHng  him  by  too  violent  a  shock. 

Electro-Diagnosis. — We  should  commence  with  faradic  shocks. 
Ordinarily  these  are  produced  in  rapid  succession  by  a  vibrating 
Neef's  hammer,  "  making "  and  "  breaking "  the  circuit  of  the 
primary  coil.  If  these  are  too  painful  to  be  borne,  we  may  often 
overcome    the  difficulty   by  loosening  the  spring  of  the   Neef's 


Anterior  crural  nerve 

Obturator  nerve 

M.  pectinajus 

M.  adductor  magnua 

M.  adduet.  longus 


M.  cruralis 


M.  vastus  iuternus  I 


M.  tensor  fascise  latae 


-  M.  sartorius 


~   ,-;   ^ -s    M.  quadriceps  femoris 

^  /    **        'Tr       (common  point) 
*-  M.  rectus  femoris 


M.  vastus  extemus 


Fig.  217.— Motor  Points  of  Anterior  Thigh  Muscles.     (Erb.) 


hammer  and  making  and  breaking  the  primary  current  by  moving 
the  spring  with  our  finger.  This  produces  an  isolated  faradic 
shock,  each  time  we  press  the  spring  into  contact  with  or  remove  it 
from  the  screw.  Such  single  shocks  are  often  tolerated  by  a  patient 
who  cannot  bear  the  ordinary  series  of  shocks  in  rapid  succession. 
In  children,  however,  it  is  sometimes  impossible  to  get  the  patient 
to  submit  even  to  single  shocks,  and  it  may  be  necessary  in  them 
to  give  a  general  ansesthetic,  in  order  to  make  an  accurate  electro- 
diagnosis. 

Whenever  possible,  we  should  compare  the  reaction  of  the 
suspected  muscles  with  that  of  other  muscles  which  are  healthy, 
preferably  the  corresponding  muscles  of  the  opposite  limb.     Of 


ELECTRO-DIAGNOSIS 


421 


course,  when  the  disease  is  bilaterally  symmetrical,  this  is  im- 
possible. An  electrical  examination,  to  be  complete,  would  have 
to  include  observations  on  every  accessible  muscle  and  motor  nerve 
in  the  body ;  tliis,  however,  is  practically  unattainable,  and  we 
usually  content  ourselves  with  selecting  a  group  of  muscles  in  the 
affected  area  and  testing  each  muscle  carefully,  both  with  faradic 
shocks  and  with  the  continuous  current,  commencing  with  the 
faradic. 

Faradic  Reactions. — Faradism    stimulates    a    muscle    most 
efficiently,  not  by  direct  action  on  the  muscle-fibres  but  through 


M.  tibial,  antic 

M.  extens.  digit,  comm. 

lonfr. 


M.  peroTifeus  breviS' 


M.  extensor  hallucis 
long. 


Mm.  interossei  dorsales  { 


Peroneal  nerve 

M.  gastrrcneni.  (outer  head) 
.M.  percnasus  longus 


M.  flexor  hallucis  long. 


M.  estens.  digit,  comm. 
hrevis 

M.  abductor  digiti  min. 


Fig.  218.— Motor  Points  of  Leg.     (Erb. 


the  motor  nerve.  To  stimulate  an  individual  muscle  by  faradism 
we  seek  for  the  place  where  the  nerve  enters  the  muscle. 
This  is  usually  a  well-defined  spot  known  as  the  "  motor  'point " 
of  the  particular  muscle.  Faradism  applied  at  such  a  "  motor 
point "  provokes  a  maximal  contraction  in  that  individual  muscle. 
The  positions  of  the  chief  "  motor  points  "  are  indicated  in  Erb's 
well-known  diagrams  (Figs.  213  to  219).  A  faradic  shock  of  a 
given  strength  produces  a  much  greater  effect  when  applied  at 
such  a  "  motor  point  "  than  when  apphed  directly  over  an  in- 
different bundle  of  muscle-fibres. 

Besides  stimulating  individual  muscles,  we  can  stimulate  whole 


422 


NERVOUS    DISEASES 


groups  by  applying  our  electrode  over  a  nerve-trunk,  such  as  the 
ulnar  or  musculo-spiral. 

--  j  In  testing  faradic  reactions  we  commence  with  feeble  shocks  and 
gradually  increase  their  strength  until  we  just  get  a  contraction 
of  the  muscle.  We  then  compare  this  contraction  with  that  pro- 
duced by  the  same  strength  of  shocks  apphed  to  a  healthy  muscle, 
preferably  the  same  muscle  of  the  opposite  limb,  if  available. 
Galvanic  Reactions. — The  galvanic  current  stimulates  a  motor 


Sciatic  nerve 

M.  biceps  fem.  (long  head) 

M.  biceps  fem.  (short  head) 

Peroneal  nerve 
M.  gastrocnem.  (outer  head) 

M.  soleus 
M.  flexor  hallucis  longus 


-  M.  glutseus  maximus 


M.  adductor  magnus 
M.  semitendinosus 
M.  se.mimenibranosus 


Posterior  tibial  nerve 

M.  gastrocnem.  (inner  head) 
M.  soleus 


M.  flexor  digitor.  comm. 
longus 

Posterior  tibial  nerve 


Fig.  219.— Motor  Points  at  back  of  Thigh  and  Leg.     (Erb.) 


nerve-fibre  at  the  moment  of  closure,  and  again  at  the  moment 
of  opening  of  the  current,  but  not  during  the  period  of  flow,  so 
long  as  the  strength  of  the  current  remains  constant.  In  the  case 
of  muscle-fibres,  galvanism  stimulates  them  at  closure  and  again 
at  opening,  and  even  throughout  the  whole  period  of  flow,  pro- 
vided the  current  be  strong  enough.  Even  when  a  nerve  is 
degenerated,  directly  applied  galvanism  is  still  able  to  produce 
contractions  in  the  muscle-fibres. 

The  "  folar  reactions  "  of  a  muscle  to  galvanism  are  of  great 
chnical  importance.     Normally,   in   a  healthy  muscle,   when  we 


ELECTRO-DIAGNOSIS  423 

stimulate  it  with  a  galvanic  current,  not  too  strong,  we  get  a 
brisk  twitch  at  closure,  then  during  the  period  of  flow  the  muscle 
remains  relaxed  until  the  current  is  suddenly  opened,  when  we  may 
get  another  twitch  at  opening.  The  contraction  at  closure  is 
greater  if  we  stimulate  with  the  kathode  (negative  pole)  than  if 
we  employ  the  anode  (positive  pole).  This  is  expressed  by  the 
formula  KCC  >  ACC  (kathodal-closure-contraction  greater  than 
anodal-closure-contraction).  To  verify  this  chnically  on  a  healthy 
muscle,  we  gradually  increase  the  strength  of  our  current  by 
means  of  the  collector.  Meanwhile,  we  make  an  occasional  double 
movement  of  the  commutator,  whereby  the  testing  pole  is 
suddenly  changed  from  kathode  to  anode  and  back  again.  Pre- 
sently, as  the  current  is  increased  in  strength  we  find  that  at 
one  position  of  this  double  movement  we  get  a  brisk  twitch  of 
the  muscle,  whilst  in  the  reverse  position  Ave  get  none.  The 
first  twitch  in  a  healthy  muscle  always  appears  at  the  kathode. 
Then  if  the  current  be  still  further  increased,  a  twitch  appears 
at  both  phases  of  the  commutator,  but  the  kathodal  contraction 
remains  the  greater.  As  a  matter  of  convenience  it  is  best  to 
employ  the  minimal  current  strong  enough  to  give  KCC,  whilst  as 
yet  there  is  no  ACC.  Meanwhile  we  notice  on  the  galvanometer 
the  number  of  milliamperes  of  current  which  are  required  to  pro- 
duce the  earhest  twitch  at  closure. 

If  the  strength  of  the  galvanic  current  be  still  further  increased 
we  obtain  a  twitch  at  opening,  the  anodal  contraction  being  pro- 
duced first  and  the  kathodal  opening  contraction  last  of  all.  The 
order  of  appearance  of  these  different  contractions  in  a  healthy 
muscle,  as  the  current  progressively  increases  in  strength,  is  there- 
fore as  follows  :  KCC  >  ACC  >  AOC  >  KOC,  and  is  indicated  in 
the  following  amplification  of  the  same  facts  : — ■ 


1. 

Weak  current 

.     KCC 

± 

Medium  current     . 

.     KCC 

ACC 

3. 

Moderately  strong  current 

.     KCC 

ACC 

AOC 

4. 

Very  strong  current 

.     KCC 

ACC 

AOC 

KOC 

Of  these  phenomena,  we  usually  concern  ourselves,  for  practical 
purposes,  only  with  the  first  two,  that  is,  with  the  contractions  on 
closure,  observing  whether  the  kathodal  closing  contraction  is 
greater  than  the  anodal  closing  contraction,  as  it  ought  to  be  in 
health. 

To  recapitulate,  in  a  normal  nerve-muscle  organ  we  obtain  a 


424  NERVOUS    DISEASES 

good  contraction  on  faradic  stimulation,  while  to  galvanism  there 
is  a  brisk  twitch  on  closure,  KCC  being  greater  than  AGO. 

Abnormalities  in  Electrical  Reactions. — Sometimes  the  ex- 
citability of  the  nerve-muscle  organ  is  increased,  both  to  faradism 
and  to  galvanism.  This  condition  of  hyper-excitability  is  met  with 
most  typically  in  tetany,  where  both  nerve  and  muscle  are  too 
easily  thrown  into  contraction.  Somewhat  similar  is  the  so-called 
"wewro^om^"  reaction,  described  by  Marina^  in  certain  cases  of 
hysteria,  by  Remak  ^  in  patients  with  progressive  muscular 
atrophy,  and  by  Handelsman^  in  syringomyelia.  This  pheno- 
menon consists  not  only  in  excessive  excitabihty  both  to  faradism 
and  galvanism,  but  also  in  a  tendency  for  the  muscle  to  remain 
in  a  state  of  tetanus  for  10  to  30  seconds  after  the  stimulus 
has  ceased.  The  phenomenon  is  not  provoked  by  stimulation  of 
the  muscle  itself,  but  only  by  excitation  of  the  nerve. 

We  sometimes  meet  with  simple  diminution  of  excitabihty,  both 
to  faradism  and  to  galvanism,  but  without  alteration  of  polar 
reactions — that  is  to  say,  KCC  remains  greater  than  ACC.  Such 
diminution  of  electrical  excitability  is  met  with  in  simple  arthritic 
muscular  atrophy,  in  the  atrophy  of  disuse  and  also  in  the  various 
myopathies,  whether  pseudo-hypertrophic  or  atrophic  in  type. 

Temporary  loss  of  faradic  excitability  occurs  in  myasthenia 
gravis,  though  not  in  every  case.  When  present,  the  myasthenic 
reaction  consists  in  the  fact  that  after  a  certain  number  of  faradic 
shocks,  the  muscle  gradually  reacts  less  and  less,  until  at  last 
it  shows  no  contraction  to  the  strongest  faradic  shocks.  We  wait 
a  few  minutes  and  then  test  again,  when  we  find  that  the  faradic 
excitability  has  reappeared,  but  can  again  be  exhausted  in  a 
similar  fashion.  The  galvanic  reactions  of  the  affected  muscles 
remain  unchanged  throughout  the  disease.  A  myasthenic  reaction 
can  also  be  produced  experimentally,  e.g.  in  the  frog's  muscles,  by 
poisoning  with  yohimbine.'*  This  suggests  that  the  phenomenon 
is  toxic  in  origin. 

During  the  paroxysms  of  the  rare  disease  known  as  family 
periodic  paralysis,  the  paralysed  muscles  are,  for  the  time,  totally 
in  excitable  either  by  faradism  or  by  galvanism.  This  is  termed 
the  cadaveric  reaction.  In  the  intervals  between  the  attacks  of 
paralysis  the  muscles  react  normally. 

1  Neurologisches  Centralhiatt,  1896,  No.  17.  ^  jj^^fi,^  jggg^  >jo_  I3, 

»  Ibid.,  1911,  s,  418.  «  Gunn,  Rev.  of  Ne^irol.  and  Psychiat.,  1908,  p.  150. 


ELECTRO-DIAGNOSIS  425 

The  myotonic  reaction  is  met  with  chiefly  in  Thomsen's  disease 
(myotonia  congenita),  but  has  also  been  observed  in  certain  types 
of  syringomyelia  accompanied  by  myotonia.  It  consists  in  the 
fact  that  on  faradic  stimulation  the  muscular  contraction  persists 
for  some  time  after  the  stimulus  has  ceased,  as  if  the  muscle,  once 
contracted,  cannot  relax.  Moreover,  in  this  disease  galvanic 
stimulation  of  the  muscle  produces  curious  wave-like  contractions, 
and  KCC  is  equal  to  instead  of  greater  than  ACC. 

Condenser  Reactions. — Condenser  discharges  are  a  valuable 
means  of  electro -diagnosis,  and  the  results  thus  obtained  can  be 
usefully  compared  with  those  observed  on  faradic  and  galvanic 
stimulation. 

The  apparatus  is  simple.  It  consists  of  a  set  of  ten  or  twelve 
condensers  of  varying  capacities,  ranging  from  0.01  of  a  micro- 
farad in  the  smallest  condenser  up  to  3.00  micro-farads  in  the 
largest.  Between  these  two  extremes  there  are  eight  or  ten  con- 
densers of  intermediate  capacity.  By  means  of  a  revolving  com- 
mutator and  a  metronome  any  one  of  these  condensers  can  be 
alternately  charged  from  the  main  and  discharged  through  the 
patient's  muscles.  The  condensers  of  different  capacities  differ 
in  one  essential  feature,  viz.  their  wave-length,  i.e.  the  duration 
of  their  discharge  through  the  body.  The  smallest  condenser  of 
the  series,  with  a  capacity  of  0.01  micro-farad,  takes  -aTF.Vro  of 
a  second  to  pass  through  the  body,  which  is  vastly  shorter  than 
the  wave-length  of  any  induction-coil,  whose  shortest  duration  is 
about  x^o-  of  a  second,  or  shghtly  less.  The  largest  condenser, 
that  with  3.00  micro-farads,  has  a  duration  of  discharge  of  xirr 
second.  Healthy  muscles  respond  to  the  smallest  condensers  of 
0.01  to  0.05  micro-farad.  As  a  muscle  degenerates,  it  requires 
impulses  of  longer  and  longer  duration,  from  condensers  of  larger 
and  larger  capacity,  to  induce  it  to  contract. 

In  this  variety  of  muscle-testing  we  place  our  electrodes  in 
position,  attach  our  box  of  condensers  to  the  main,  set  the  metro- 
nome going,  and  then,  by  moving  a  key  over  successive  studs 
on  the  switchboard,  we  find  out  the  smallest  condenser  which  just 
causes  the  muscle  to  contract  and  produces  the  first  flicker  of 
response.  The  process  of  testing  by  means  of  condensers,  unlike 
faradic  or  galvanic  testing,  is  entirely  painless,  the  only  sensation 
produced  being  that  of  the  sudden,  muscular  twitch.  Moreover, 
it  is  unnecessary  to  decide  whether  the  contraction  produced  by 


426  NERVOUS    DISEASES 

the  condenser  discliarge  is  brisk  or  sluggish,  strong  or  weak.  All 
we  have  to  decide  is  whether  the  muscle  contracts  at  all,  and,  if 
so,  to  which  condenser. 

In  healthy  muscles,  contractions  are  produced  by  the  smallest 
condensers  of  the  series,  viz.  from  0.01  to  0.02  micro-farad. 

Reactions  of  Degeneration. — By  far  the  most  important  modi- 
fication of  electrical  reactions  is  the  condition  known  as  the 
"  reactions  of  degeneration,"  or  colloquially  as  R.D.  This  condition 
is  present  when  the  nerve-muscle  organ  has  undergone  degenera- 
tion, from  disease  or  destruction  of  the  spino -muscular  motor 
neurone.  As  a  result  of  such  a  lesion,  the  motor  nerve-fibre  dis- 
integrates within  a  few  days  and  loses  its  power  of  conducting 
impulses.  The  corresponding  muscle-fibre  undergoes  important 
changes ;  it  loses  its  fibrillar  or  anisotropic  element,  the  element 
which  contracts  with  a  brisk  twitch  and  carl  be  stimulated 
with  a  faradic  shock ;  whilst  it  retains  only  its  sarcoplasm,  a  less 
excitable  element,  which  contracts  slowly  and  can  still  be  stimu- 
lated by  galvanism  and  by  condenser  shocks  of  a  slow  wave- 
length. 

In  a  typical  case  the  phenomena  are  as  follows  : — to  famdism 
there  is  no  response,  since  the  nerve  has  degenerated  ;  to  galvanism 
the  muscle-fibres  still  respond — in  fact  for  a  short  time  they  become 
hyperexcitable,  contracting  to  a  weaker  current  than  in  health. 
But  their  polar  reactions  are  altered.  The  anodal  contraction  on 
closure  is  now  equal  to,  or  greater  than  the  kathodal  (ACC  >  KCC). 
Moreover,  what  is  equally  characteristic,  the  response  of  the 
muscle  is  no  longer  a  brisk  twitch  ;  it  is  a  slow,  sluggish,  almost 
vermicular  movement. 

In  cases  yielding  complete  R.D.  by  farado-galvanic  methods, 
if  we  examine  the  muscles  by  condenser  discharges  we  find  that, 
instead  of  giving  a  response  to  condensers  of  0.01  to  0.02  micro- 
farad, they  will  not  respond  to  condensers  smaller  than  0.50  micro- 
farad, and  may  require  1.00,  2.00,  or  even  3.00  micro-farads,  i.e. 
an  impulse  whose  duration  is  from  100  to  300  times  as  long  as 
that  required  in  health. 

If  a  nerve  be  divided,  the  reactions  of  degeneration  do  not 
appear  at  once.  It  is  only  after  some  ten  days  or  so  that  they 
develop.  Once  established,  the  reactions  of  degeneration  per- 
sist, unless  the  nerve  regenerates  and  re-establishes  a  connec- 
tion between  the  muscle  and  the  motor  nucleus.     In  the  process  of 


ELECTRO-DIAGNOSIS  427 

recovery,  voluntary  motor  power  reappears  before  faradic  excita- 
bility returns.  In  many  cases  recovery  does  not  take  place  and  the 
nerve-muscle  organ  remains  permanently  degenerated,  as,  for 
example,  when  the  motor  nucleus  in  the  cord  or  medulla  is  de- 
stroyed, or  when  a  nerve-trunk  is  completely  divided  and  its  ends 
have  not  been  reunited. 

In  certain  cases  we  meet  with  partial  or  incomplete  reactions  of 
degeneration.  These  consist  in  a  sluggish  contraction  to  galvanism, 
ACC  being  greater  than  KCC,  but  the  reaction  to  faradism  is  not 
lost,  but  only  diminished.  This  condition  indicates  a  less  severe 
injury  of  the  nerve-fibres  than  if  typical  R.D.  be  present. 

Conditions  of  partial  R.D.  can  be  further  differentiated  into 
those  of  mild  and  severe  degree,  according  to  the  response  of  the 
muscle  to  condenser-shocks  of  increasing  wave-lengths.  As  a 
muscle  degenerates,  instead  of  responding  to  condensers  of  0.01 
to  0.02  micro-farad,  larger  condensers  of  0.25  or  0.50  micro-farad, 
with  longer  wave-lengths,  are  required. 

Sometimes  we  have  mixed  reactions,  some  fibres  of  a  muscle 
retaining  their  normal  reactions  whilst  adjacent  fibres  have  reac- 
tions of  degeneration.  This  is  best  exemplified  by  cases  of 
progressive  muscular  atrophy  where  degenerated  muscle-fibres  are 
interspersed  amongst  the  healthy. 

To  sum  up,  then,  the  presence  of  R.D.  always  indicates  a  lesion 
somewhere  in  the  lower  or  spino-muscular  motor  neurone.  We 
should  be  careful  to  wait  ten  days  or  a  fortnight  from  the  onset 
of  the  paralysis  before  giving  a  verdict,  inasmuch  as  we  have 
seen  that  it  takes  some  time  for  degeneration  to  become  estab- 
lished. R.D.  occur  in  lesions  of  peripheral  motor  nerves,  also  in 
gross  nuclear  diseases  such  as  acute  anterior  poHomyehtis,  haemor- 
rhage or  thrombosis  in  the  anterior  cornua  or  motor  nuclei.  Mixed 
reactions,  on  the  other  hand,  are  found  in  progressive  muscular 
atrophy  and  in  bulbar  palsy,  where  the  nerve-cells  of  the  motor 
nuclei  are  picked  out  one  by  one,  leaving  adjacent  nerve-cells 
unaffected. 

Electro-Prognosis. — In  many  paralyses  due  to  organic  lesions 
of  peripheral  motor  nerves  (of  which  the  commonest  instance  is 
that  of  a  neuritis  of  the  facial  nerve),  it  is  of  importance  to  be  able 
to  estimate  not  only  the  degree  of  degeneration  which  has  occurred, 
but  also  the  prospects  of  recovery.  To  make  an  accurate  prognosis 
we  must  wait  at  least  ten  days,  and  preferably  a  fortnight,  before 


428  NERVOUS    DISEASES 

making  our  investigation,  so  as  to  allow  time  for  degenerative 
changes  to  have  occurred.  Electrical  examination  at  any  earlier 
date  is  practically  valueless  for  purposes  of  prognosis.  If,  after  a 
fortnight's  motor  palsy — say,  in  a  case  of  Bell's  paralysis — we  get 
typical  R.D.,  the  degeneration  of  the  nerve  is  severe  and  recovery 
will  not  commence  for  three  months  at  least,  possibly  not  for  a  year, 
and  the  patient  may  even  remain  permanently  paralysed.  And 
at  the  best,  if  recovery  does  occur,  it  will  probably  be  imperfect 
and  associated  with  some  contracture.  If  partial  R.D.  be 
present,  the  prognosis  is  less  grave  and  recovery  may  be  expected 
within  six  or  eight  weeks.  If  the  reactions  be  normal,  or  if  there 
be  simply  a  diminution  to  faradism  and  galvanism,  but  without 
polar  changes,  recovery  may  be  looked  for  in  from  three  to  six 
weeks,  or  even  sooner. 


CHAPTEll   XXIII 

THE   OEREBRO-SPINAL  FLUID 

The  cerebro-spinal  fluid  is  secreted  by  the  glandular  ependymal 
cells  covering  the  choroid  plexuses.  It  flows  from  the  ventricles 
into  the  sub-arachnoid  space,  bathing  the  brain  and  spinal  cord. 
The  total  amount  of  fluid  normally  present  is  estimated  at  from 
100  to  150  cubic  centimetres.  Normally  the  fluid  is  constantly 
secreted  in  a  quantity  sufficient  to  replace  that  which  is  continually 
reabsorbed  into  the  general  circulation,  partly  by  way  of  the 
lymphatics,  veins,  and  intra-cranial  sinuses  of  the  dura  mater, 
and  partly  by  osmotic  diffusion  through  the  sub-arachnoid  space. 
In  cases  of  cranial  or  spinal  injury  when  the  subarachnoid  space 
is  in  communication  with  the  surface,  as  much  as  2  to  4  litres  daily 
have  been  observed  to  escape.  In  some  patients,  as  St.  Clair 
Thompson  and  others  have  shown,  a  spontaneous  flow  of  cerebro- 
spinal fluid  occurs  through  the  cribriform  plate  and  drips 
constantly  from  the  nose. 

The  posterior  lobe  of  the  pituitary  body  pours  its  secretion 
through  the  hollow  infundibulum  into  the  cerebro-spinal  fluid  of 
the  third  ventricle.  Experiments  by  Gushing  and  Goetsch  ^  have 
demonstrated  that  normal  cerebro-spinal  fluid  contains  a  substance 
which  gives  the  same  reaction  as  extracts  of  the  pars  nervosa  itself. 
The  fluid  receives  various  products  of  metabolism  from  the  nerve- 
centres.  It  may  undergo  changes  in  lesions  of  these  centres  or  of 
their  meninges  ;  hence  the  clinical  importance  of  its  examination. 

Various  drugs,  taken  by  the  mouth,  can  be  detected  in  the 
cerebro-spinal  fluid.  Thus  urotropin  taken  by  the  mouth  can  be 
shown  to  yield  formic  aldehyde  in  the  fluid,  whilst  in  acute  alco- 
holic poisoning  alcohol  can  be  demonstrated  in  the  fluid,  in  a  pro- 
portion of  from  1.5  to  4  per  cent.,  within  two  or  three  hours  after 
the  alcohol  has  been  taken.  In  dehrium  tremens,  on  the  other 
hand,  due  to  sudden  withdrawal  of  alcohol  in  a  chronic  alcohohc 
subject,  the  cerebro-spinal  fluid  contains  little  or  no  alcohol. 

1  Am.  J.  of  Physiology,  1910,  vol.  xxvii.  p.  60. 
429 


430 


NERVOUS    DISEASES 


12  Th 


In  the  adult,  tlie  spinal  cord  terminates  at  the  level  of  the  lower 
part  of  the  first  lumbar  vertebra.  Below  that  level  the  arachnoidal 
sac  extends  as  a  hollow  cavity  as  low  down  as  the  second  sacral 
vertebra  (see  Fig.  220).  There  is  thus  a  considerable  extent  of 
arachnoidal  cavity  devoid  of  spinal  cord,  occupied  simply  by  the 

roots  of  the  cauda  equina  and  by  the 
cerebro-spinal  fluid  which  bathes 
them.  From  this  region  we  can 
withdraw  cerebro-spinal  fluid  with- 
out risk  of  injury  to  the  spinal 
cord.  In  order  to  do  so,  we 
enter  the  cerebro-spinal  cistern 
from  behind,  somewhere  between 
the  laminae  of  the  second  lumbar 
and  the  second  sacral  vertebra. 

The  two  widest  inter-laminal 
spaces  are  the  one  between  the 
third  and  fourth,  and  the  other 
between  the  fourth  and  fifth 
lumbar  laminae.  Of  these  we  usu- 
ally select  the  space  between  the 
fourth  and  fifth  laminae,  because, 
as  a  rule,  it  is  slightly  the  larger. 
These  two  inter-laminal  spaces  are 
very  easily  found  as  follows  :  we 
draw  a  horizontal  line  across  the 
patient's  back,  at  the  level  of  the 
highest  margin  of  the  iliac  crests. 
,,  ^.  This  line  intersects  the  vertebral 

Fig.  220. — (After  Kaymond.)  Diagram  i  •         j-      i        <•  i 

of  lower  end  of  vertebral  column  and    Column    at    the    tip    ot    the    tourth 


Direction  of 
needle  during 
lumbar 
cj  J       puncture 


its  relations  to  the  spinal  cord  and 
Cauda  equina.  The  double-shaded 
portion  of  the  cord  is  the  conus  ter- 


lumbar    spine.      We     make     our 
puncture  immediately  below  this 

minalis,  with  which  the  filum  ter-    „-^:„„   l'U\nc    001  \ 
,    .  ,.  buiiit;   iJJiy.  ZiZiii. 

minale  is  continuous.  ^  .      °  . 

It  is  convenient  to  use  an  all- 
glass  syringe  which  is  readily  sterihsable  on  which  to  mount 
our  needle,  which  should  be  of  fairly  large  calibre.  The  needle 
itself  is  made  of  platinum  and  iridium,  which  is  less  liable  to 
snap  and  can  also  be  boiled  without  rusting,  unhke  a  steel  needle. 
It  must  be  long  enough  to  reach  into  the  arachnoidal  sac,  and  yet 
short  enough  to  stop  short  "within  the  sac  without  penetrating  to 


THE    CEREBRO-SPINAL    FLUID 


431 


the  dura  on  the  far  side.  For  this  purpose  the  most  suitable 
length  of  needle  is  about  8  centimetres,  or  just  over  three 
inches. 

As  to  the  patient's  posture  during  the  operation  of  "thecal 
puncture,"  he  may  be  lying  on  a  bed  or  couch,  in  the  left  lateral 
position,  with  the  knees  and  shoulders  approximated.  But  it  is 
better,  if  possible,  to  have!  him  sitting  on  a  low  seat,  stoop- 
ing well  forwards,  with  his  knees  separated,  his  arms  hang- 
ing loose,  and  his  hands  touching  the  ground.  In  this' way,  the 
laminaB  are  separated  to 
their  utmost  extent  (see 
Fig.  221). 

We  carefully  steriUse  the 
skin  at  the  site  of  puncture 
and  render  it  ansesthetic 
by  means  of  a  spray  of 
ethyl  chloride.  The  operator 
places  his  left  index  finger 
on  the  fourth  lumbar  spine 
as  a  guide,  and  with  his 
right  hand  pushes  in  the 
needle,  about  half  an  inch 
below  and  half  an  inch  to 
the  right  of  this  spot  (so  as 
to  avoid  the  dense  inter- 
spinous  ligament),  directing 
the  point  of  the  needle 
horizontally  forwards  and  a 

Uttle  inwards.  The  ligamentum  subflavum,  deep  in,  between  the 
laminae,  is  somewhat  resistant,  and  the  needle  is  felt  to  be  checked 
here.  But  we  push  firmly  on,  if  no  bone  is  struck,  and  suddenly 
the  needle  penetrates  the  ligament  and  dura-arachnoid  and  is  now 
in  the  arachnoidal  sac  (see  Fig.  222).  If  we  strike  on  a  lamina 
instead  of  the  ligament,  we  withdraw  shghtly  and  try  a  point 
above  or  below. 

Sometimes  during  the  operation  the  patient  feels  a  sudden, 
sharp  pain  shooting  down  his  right  thigh  and  leg.  This  simply 
means  that  our  needle  has  touched  one  of  the  roots  of  the  cauda 
equina  en  route,  and  is  of  no  other  significance. 

We  now  detach  the  syringe  and  allow  the  cerebro-spinal  fluid 


Fig.  221. — Lumbar  puncture.     Fluid  drop- 
ping from  needle  into  test-tube. 


432 


NERVOUS    DISEASES 


to  escape  through  the  needle,  collecting  from  3  to  5  c.c.  in  a 
sterilised  test-tube.  It  is  better  not  to  employ  suction  bj  the 
syringe,  unless  some  difficulty  be  experienced  in  getting  the  fluid 
to  run.  The  pressure  of  the  fluid  as  it  escapes  may  be  measured, 
if  desired,  by  means  of  a  rubber  tube  with  a  manometer  attached. 
Normally  the  fluid  trickles  out  slowly,  drop  by  drop,  at  the  rate 
of  about  60  drops  per  minute.  The  first  few  drops  should  be  dis- 
carded, since  they  may  be  mixed  with  blood  from  our  needle-wound 
of  the  superjacent  tissues. 

Occasionally  it  happens  that  even  when  we  have  successfully 
penetrated  within  the  ligamentum  subflavum,  no  fluid  will  flow. 


ComnixiTv  IbioLc  Artertes. 


■IrLferiorJ'encxy  Comoj. 

Burcu  J^outer. 

QuajdratasLuwJborvjw. 


•ErectxirSpijiae . 


Fig.  222. — Horizontal  .section  at  the  level  of  the  fourth  lumbar  vertebra, 
showing  the  relations  of  the  parts  concerned  in  thecal  puncture. 

This  is  usually  due  to  blocking  of  the  needle  by  a  small  plug 
of  blood-clot  or  shred  of  muscle  or  connective-tissue,  during  the 
process  of  puncture.  Or  it  may  be  due  to  one  of  the  cauda 
equina  roots  floating  against  the  end  of  the  needle.  Such  con- 
ditions are  easily  rectified  by  passing  a  steriHsed  stilette  along  the 
needle,  to  clear  it.  Sometimes  it  happens  that  the  needle  pierces 
the  hgamentum  subflavum  but  pushes  the  spinal  theca  in  front  of 
it,  so  that,  even  though  the  stilette  shows  the  needle  to  be  free  from 
obstruction,  no  fluid  comes.  In  such  cases  it  is  best  to  withdraw 
the  needle  and  puncture  at  the  next  space  above. 

The  normal  pressure  of  the  cerebro- spinal  fluid,  in  the  recumbent 
posture,  is  from  10  to  15  centimetres  of  water.  In  the  sitting 
position  it  is  higher,  amounting  to  20  to  25  centimetres.  Coughing 
causes  a  slight  elevation  of  2  to  4  centimetres.     Respiratory  varia- 


THE    CEREBRO-SPINAL   FLUID  433 

tions  are  not  noticeable  in  the  normal  subject,  but  in  cases  in 
which  the  intra-thecal  pressure  is  increased  to  30  centimetres  and 
upwards,  slight  respiratory  waves  may  occur,  not  amounting  to 
more  than  2  or  3  centimetres. 

Sometimes  the  intrathecal  pressure  is  increased,  so  that  the  fluid 
escapes  in  a  jet,  instead  of  drop  by  drop.  This  occurs  chiefly  with 
intra-cranial  tumours  and  in  the  various  forms  of  meningitis, 
although  even  in  these  conditions  an  increased  pressure  of  fluid 
in  the  lumbar  region  is  by  no  means  constant,  for  sometimes  in 
meningitis  there  is  occlusion  of  the  foramen  of  Magendie,  or  of 
the  foramina  of  Key  and  Retzius,  or  the  cerebellum  may  be 
partially  impacted  in  the  foramen  magnum,  cutting  oft"  the 
intra- ventricular  from  the  spinal  pond. 

The  fluid  may  be  accidentally  mixed  with  blood  from  the  wound- 
ing of  an  arachnoidal  vein  during  the  puncture  ;  this  is  an  accident 
which  cannot  be  guarded  against.  In  most  cases  such  local  bleed- 
ing clears  up  after  a  few  seconds,  the  fluid  becoming  progressively 
clearer  and  clearer.  But  admixture  of  blood  also  occurs  in  cases  of 
pre-existent  subarachnoid  haemorrhage,  cerebral  or  spinal,  as  in  frac- 
ture of  the  skull,  intra-ventricular  haemorrhage,  or  in  trauma  of  the 
spinal  cord.  We  can  usually  distinguish  between  haemorrhage 
due  to  the  local  puncture  and  haemorrhage  which  results  from 
a  previous  intra-thecal  lesion.  We  do  this  by  centrifuging  the 
fluid.  In  local  haemorrhage  due  to  puncture,  the  blood  corpuscles 
fall  to  the  foot  of  the  centrifuge-tube,  leaving  the  superjacent 
fluid  clear  and  limpid,  whereas  in  a  pre-existing  cerebral  or  spinal 
haemorrhage  the  fluid  (which  during  its  flow  is  equaUy  tinged 
from  start  to  finish,  and  generally  less  deeply  tinged  than  in  local 
haemorrhage)  remains  of  a  yellow  colour  even  after  centrifuging 
(xanthochromia) . 

In  most  cases  the  withdrawal  of  a  small  quantity  of  cerebro- 
spinal fluid  causes  the  patient  no  discomfort.  But  in  a  small  pro- 
portion of  cases  he  may  complain  of  severe  headache,  appearing 
an  hour  or  two  later,  and  lasting  perhaps  for  several  days.  This 
is  most  often  the  case  in  patients  who  walk  about  as  usual  after 
the  puncture,  and  headache  can  generally  be  prevented  by  recom- 
mending the  patient  to  rest  for  a  day  or  so,  or  at  least  to  avoid 
physical  exertion. 

Normal  cerehro-S'pinal  fluid  is  absolutely  colourless,  like  water. 
It  is  an  alkaline,  saline  fluid  with  a  specific  gravity  of  1006  to  1008. 

2  E 


434  NERVOUS    DISEASES 

It  contains  sodium  chloride,  together  with  a  trace  of  serum-globuhn 
and  of  albumose  (the  total  albumin  being  from  0.025  to  0.05  per 
cent.),  and  also  a  substance  which  reduces  Fehling's  solution  and 
forms  osazone  crystals.  Microscopically  it  contains  a  few  large, 
fiat,  endothelial  plates,  and  perhaps  an  occasional  lymphocyte. 
It  contains  no  organisms. 

The  Diagnostic  Significance  of  Cerebro-spinal  Fluid.— For 
diagnostic  purposes  the  fluid  may  be  examined  in  various 
ways. 

(1)  Physical  Characters. — Instead  of  being  clear  and  limpid 
like  water,  the  fluid  may  be  opalescent,  turbid,  cloudy,  or  even 
purulent,  as  in  some  cases  of  meningitis.  In  severe  jaundice  it 
has  been  observed  to  be  yellow  and  clear,  whilst  in  cases  of  recent 
haemorrhage  either  into  the  brain  or  cord  it  may,  as  we  have  men- 
tioned, be  blood-stained.  In  haemorrhages  of  older  date,  say  a 
week  or  more,  the  fluid  may  be  of  a  clear  yellow  colour — xantho- 
chromia. The  coexistence  of  xanthochromia  with  spontaneous 
coagulation  of  the  fluid  on  standing  generally  points  to  chronic 
compression  of  the  spinal  cord  (see  later,  p.  435). 

The  mere  absence  of  cloudiness  or  coloration,  however,  does  not 
necessarily  mean  that  the  fluid  is  healthy,  since  we  obtain  perfectly 
clear  cerebro-spinal  fluid  in  such  diseases  as  tabes,  general  paralysis, 
and  certain  forms  of  meningitis. 

In  cases  of  sudden  hemiplegia  we  are  sometimes  in  doubt 
whether  the  lesion  is  haemorrhage  or  thrombosis.  The  diagnosis 
between  these  two  conditions  may  be  very  difficult.  But  the 
treatment  of  the  two  is  diametrically  opposite.  In  a  case  of 
thrombosis  we  stimulate,  and,  if  necessary,  push  our  anti- 
syphilitic  remedies,  whereas  in  cerebral  haemorrhage  we  try  to 
lower  the  intra-cranial  blood-pressure  and  diminish  the  force  of 
the  heart.  If  in  a  doubtful  case  we  perform  lumbar  puncture  and 
obtain  blood-stained  fluid,  or  fluid  which  has  a  yellow  tinge  even 
after  centrifuging,  the  diagnosis  is  simplified.  In  traumatic  cases 
this  is  of  great  value  in  indicating  the  presence  of  subarachnoid 
intra-cranial  haemorrhage.  Cathcart  of  Edinburgh  ^  recorded  a 
case  in  which,  after  a  head  injury,  examination  of  the  cerebro- 
spinal fluid  helped  to  settle  the  diagnosis  of  intra-cranial  haemor- 
rhage. He  trephined,  tied  the  ruptured  artery,  and  saved  the 
patient's    life.      But  in  compound  fracture  of  the  skull  lumbar 

1  Scot.  Med.  and  Surg.  Journ.,  Edinburgh,  1902,  p.  145. 


THE    CEREBRO-SPINAL   FLUID  435 

puncture  may  yield  nothing,   if  the  fluid  happens  to  be  escaping 
by  other  channels,  viz.  through  the  lacerated  membranes. 

(2)  Chemical  Characters. — These  are  of  value.  Thus,  for 
example,  a  marked  excess  of  albumin  is  found  in  acute  meningitis, 
and  to  a  lesser  degree  in  tabes  and  in  general  paralysis  of  the  insane, 
the  protsid  concerned  in  tabes  and  general  paralysis  being  eu- 
globulin.  One  method  of  examining  for  globulin  is  by  Noguchi's 
test,^  which  is  performed  as  follows  : — 

To  two  parts  of  cerebro-spinal  fluid  are  added  five  parts  of  a  10  per 
cent,  solution  of  butyric  acid  in  normal  saline  solution.  This  mixture 
is  heated  to  boiling-point,  and  then  one  part  of  a  normal  (4  per  cent.) 
solution  of  sodium  hydrate  is  added  and  the  mixture  is  again  boiled 
briefly.  After  standing  for  two  to  thirty  minutes,  if  a  globulin  be 
present,  there  is  a  flocculenfc  or  granular  precipitate. 

A  simpler  method  of  detecting  globulin  (and  one  which  is  free 
from  the  oHactory  discomfort  of  Noguchi's  method)  is  by  means 
of  ammonium  sulphate.^ 

On  to  the  surface  of  a  saturated  solution  of  ammonium  sulphate  in 
a  test-tube  a  small  amount  of  cerebro-spinal  fluid  is  allowed  to  flow 
by  means  of  a  fine  pipette.  If  globulin  be  present,  a  fine  white  ring 
appears  at  the  junction  of  the  two  fluids. 

The  Nonne-Apelt  test  consists  in  mixing  together  equal  quantities 
of  cerebro-spinal  fluid  and  saturated  solution  of  ammonium  sulphate, 
and  shaking  them  together.  If  globuHn  be  present,  cloudiness  appears 
within  three  minutes. 

In  some  cases  this  excess  of  protein  is  so  great  that  the  fluid, 
on  standing,  coagulates  into  a  jelly-like  clot,  usually  of  a  golden 
yellow  colour.  This  is  always  pathological,  and  has  been  found  in 
cert.ain  tumours  of  the  spinal  cord  or  meninges,  and  even  in  cerebral 
tumours.  It  is  not  necessarily  accompanied  by  any  excess  of  cells. 
It  has  also  been  observed  in  syphilitic  or  tuberculous  meningitis,  in 
which  conditions  there  is  superadded  an  increase  in  the  lymphocyte 
content.''^  This  combination  of  massive  coagulation  with  xantho- 
chromia is  apparently  due  to  compression  of  the  spinal  cord  with 
damming  up  of  the  cerebral  from  the  spinal  fluid. 

In  acute  meningitis,  whether  tuberculous  or  pyogenic,  sugar  is 
almost  always  absent,  the  sugar  being  broken  up  by  the  organisms, 
with  the  formation  of  lactic  acid.     Hence  the  alkalinity  of  the  fluid 

^  Jouriml  of  Experimental  Medicine,  1909,  vol.  xi.  p.  84. 
2  Jones,  Reviciv  of  Neurol,  and  Psychiatry,  1909,  p.  379. 

^  Raven,  Deutsch.  Zeitsch  f.  NervenheilJcunde,  1912,  Bd.  44,  s.  381.  Green- 
field, Lancet,  1912,  ii.  p.  685. 


436  NERVOUS    DISEASES 

is  reduced.  In  clironic  meningitis,  in  tabes,  and  in  general  paralysis 
of  the  insane,  sugar  is  often  diminished. 

The  Wassermann  reaction  in  the  cerebro-spinal  fluid  (consisting 
in  an  abnormal  fixation  of  the  blood-serum  complement,  whereby 
the  normal  haemolysis  no  longer  occurs  in  the  presence  of  red 
blood-corpuscles)  is  frequently  of  great  diagnostic  value.  In 
cerebro-spinal  syphilis,  whether  of  meningo -vascular  type  or  of  the 
parenchymatous  type,  as  in  tabes  and  general  paralysis,  the  reaction 
is  positive  in  varying  proportions.  Thus  in  general  paralysis  and 
tabo -paralysis  it  is  positive  in  from  98  to  100  per  cent,  of  cases, 
in  tabetics  in  from  48  to  50  per  cent.,  and  in  meningo-vascular 
cerebro-spinal  syphilis  in  from  8  to  25  per  cent.,i  being  more  marked 
in  affections  of  the  spinal  than  of  the  cerebral  meninges. 

In  cases  of  uraemia  the  cerebro-spinal  fluid  may  contain  urea 
in  quantities  of  0.1  to  0.2  per  cent.,  or  even  higher.^ 

A  simple  chemical  test  for  meningitis  is  by  means  of  a  solution 
of  potassium  permanganate  (0.1  per  cent.).^  Equal  parts  of  cerebro- 
spinal fluid  and  permanganate  solution  are  mixed  in  a  test-tube. 
With  normal  cerebro-spinal  fluid  the  colour  of  the  mixture  remains 
pink.  If  meningeal  changes  be  present,  however,  the  perman- 
ganate becomes  reduced,  and  a  yellow  or  brown  colour  appears 
within  two  or  three  minutes.  This  reaction  can  also  be  carried  out 
as  a  "  ring-test,"  the  permanganate  solution  being  carefully  poured 
on  the  top  of  the  cerebro-spinal  fluid.  The  brown  and  yellow 
zones  then  appear  at  the  junction  of  the  two  fluids. 

Lange's  colloidal  gold  reaction  ■*  also  enables  us  to  detect  the 
presence  of  inflammatory  changes  in  the  cerebro-spinal  fluid.  It 
further  indicates  whether  these  are  syphilitic  in  origin  or  due  to 
other  varieties  of  infection.  Only  a  small  quantity  of  cerebro- 
spinal fluid  (0.2  c.c.)  is  required  for  the  test,  which  is  carried  out 
as  follows  : — 

To  a  litre  of  freshly-distilled  water  are  added  10  c.c.  of  a  1  per  cent, 
solution  of  chloride  of  gold,  together  with  5  c.c.  of  a  5  per  cent,  solution 
of  glucose.  This  is  heated  to  boiling  point,  and  then,  drop  by  drop, 
to  the  boiling  fluid,  is  added  a  5  per  cent,  solution  of  caustic  potash, 

1  Mott,  Brit.  Med.  Journal,  Nov.  18,  1911,  p.  1337. 
Eichelberg,  Neurologisches  Centralblatt,  1912,  p.  931. 
Head  and  Fearnsides,  Brain,  1914,  vol.  xxxvii.  p.  79. 

2  Soper  and  Grant,  Archives  Int.  Med.,  1914,  p.  131. 

3  Boveri,  Munchener  med.  Wochenschrift,  1914,  June  2,  p.  1215. 
*  Lange,  Berlin  Jclin.  Wochensch.,  1912,  No.  19. 

Eicke,  Munch,  med.  Wochensch.,  1913,  No.  49. 


THE    CEREBROSPINAL    FLUID  437 

until  a  deep  red  coloui-  is  produced.  This  is  usually  ubtained  with 
from  3.6  to  4  c.c.  of  KOH  solution.  All  the  above-mentioned  reagents 
must  be  made  with  freshly-distilled  water,  using  vessels  of  specially 
pure  glass,  free  from  any  trace  of  soda,  sterilised  in  distilled  water. 
If  the  resulting  solution  has  a  blue  tinge,  it  is  useless.  It  must  be 
deep  red. 

A  row  of  10  or  12  narrow  test-tubes  is  set  up  in  series.  Into  the 
first  of  these  we  place  1.8  c.c.  of  a  0.4  per  cent,  solution  of  Na.Cl.  (made 
up  with  freshly-distilled  sterilised  water),  together  with  0.2  c.c.  of 
cerebro-spinal  fluid,  constituting  a  1/10  dilution.  In  each  of  the  re- 
maining tubes  of  the  series  we  place  1  c.c.  of  Na.Cl.  solution.  From 
the  first  tube  (which  contains  2  c.c.  of  a  1/10  dilution)  we  now  remove 
I  c.c.  by  means  of  a  pipette,  and  transfer  it  to  the  second  tube,  thus 
making  a  dilution  of  1/20.  After  thorough  mixing,  we  again  transfer 
1  c.c.  from  the  second  to  the  third  tube,  making  a  dilution  of  1/40, 
and  so  on,  throughout  the  series  of  tubes,  obtaining  dilutions  of  1/10, 
1/20,  1/40,  1/80,  1/160,  1/320,  &c.,  down  to  1/20,000.  To  eacli  of 
these  tubes,  containing  1  c.c.  of  progressively  diluted  cerebro-spinal 
fluid,  we  now  add  5  c.c.  of  the  gold  solution.  The  whole  technique 
is  carried  out  in  about  five  minutes. 

Normal  cerebro-spinal  fluid  gives  a  negative  reaction,  i.e.  in 
all  the  tubes  the  red  colour  remains  unchanged,  even  after  standing 
twenty-four  hours.  If  inflammatory  changes  are  present,  however, 
the  albuminoid  substances  precipitate  the  gold,  changing  the  colour 
from  the  original  red  to  a  bluish  red,  to  hlac,  dark  blue,  pale  blue, 
or  even  to  a  colourless  solution.  In  the  latter  instance  the  precipi- 
tated gold  falls  down  as  a  blue-black  precipitate.  We  might  expect 
this  decolourisation  to  be  proportional  to  the  concentration  of  the 
cerebro-spinal  fluid  and  to  diminish  steadily  according  to  the 
dilution.  This,  however,  is  not  so.  Each  pathological  fluid  has 
its  curve  of  precipitation—"  gold-curve,"  whose  maximum  hes  at 
a  special  place  in  the  series  of  dilutions.  In  syphihtic  infection 
of  the  fluid  the  maximum  of  the  curve  occurs  at  dilutions  of  1/40 
to  1/80  (see  Fig.  223).  Stronger  or  weaker  dilutions  produce  no 
precipitation  of  gold.  This  curve  is  pathognomonic  of  syphihs. 
The  syphihtic  gold  curve  occurs  also  in  tabes.  Other  diseases 
associated  with  albumin  in  the  cerebro-spinal  fluid  yield  quite 
different  curves,  in  which  the  maximum  is  displaced  to  the  right, 
so  that  with  the  stronger  concentrations  the  gold  solution  remains 
unchanged,  the  maximum  of  the  curve  occurring  further  down  the 
series. 

In  general  paralysis  the  gold  curve  appears  different,  inasmuch 
as  all  the  tubes  from  1/10  to  1/640  are  completely  decolourised. 


438 


NERVOUS    DISEASES 


Nevertlieless  we  observe,  immediately  after  adding  the  gold  solu- 
tion, that  precipitation  always  begins  first  at  1/40  and  1/80,  just 
as  in  cerebro-spinal  syphilis,  whilst  in  the  other  tubes  of  the  series 
it  occurs  much  more  gradually. 

The  addition  of  hlood-serum  to  a  normal  cerebro-spinal  fluid 
gives  a  curve  whose  maximum  is  displaced  considerably  to  the 
right,  when  compared  with  the  syphilitic  gold-curve.     Thus  the 


10 


Red 


Blue  Red 


Violet. 


Blue. 


Pale  Blue. 


White. 


20 


1 
4d 


Dilution. 
_L  J- 

80  160 


1 

320 


1 
640 


1 
1280 


1 
2560 


' 

X 

r 

^ 

\ 
\ 

1 

\ 

\ 

\ 

^ 

\ 

/ 

• 
• 

\ 

} 

1.  Gold-curve  in  cerebro-spinal  syphilis  and  tabes 

2.  „        ,,        general  paralysis. 

„  /normal  cerebro  spinal  fluid  mixed  with  blood  serum 

■',       "      ( tuberculous  meningitis. 
4.        ,,        ,,        purulent  meningitis  and  cerebral  abscess. 

Fig.  223.— Lance's  Gold  Eeaction. 


accidental  contamination  of  cerebro-spinal  fluid  with  traces  of 
blood  during  the  puncture  does  not  obscure  a  syphilitic  curve  if 
present. 

Tuberculous  meningitis  gives  the  same  curve  as  blood-mixed 
fluid,  whereas  furulent  meningitis  and  hrain  abscess  give  a  still  more 
pronounced  "  meningitic "  curve,  whose  maximum  is  always  to 
the  right  of  the  syphilitic. 

(3)  Bacteriological  Characters. — These  are  chiefly  of  value  in 
cases  of  meningitis,  to  determine  the  particular  organism  causing 
the  disease.  Thus,  for  example,  in  epidemic  cerebro-spinal 
meningitis  the  meningo-coccus  {diplococcus  intra- cellularis)  is  found  ; 
in  tuberculous  meningitis,  the  tubercle  bacillus  ;    and  in  other 


THE    CEREBRO-SPINAL    FLUID  439 

varieties  of  meningitis  we  may  find  staphylococci,  streptococci, 
pneumococci,  and  so  on.  We  should  remember  that  failure  to 
discover  tubercle  bacilli  does  not  necessarily  exclude  tuberculous 
meningitis,  though  their  presence  confirms  such  a  diagnosis. 


To  demonstrate  the  bacilli  in  tuberculous  meningitis  it  is  con- 
venient to  allow  the  fluid  to  stand  from  12  to  24  hours,  by  which 
time  a  fine  coagulum  has  usually  formed.  This  is  removed  by  a 
needle,  spread  on  a  slide,  fixed  and  stained  in  the  usual  manner. 

In  doubtful  cases  inoculation  experiments  on  guinea-pigs  are  of 
value.  In  Landry's  ascending  paralysis  various  organisms  (tetra- 
cocci  and  others)  have  occasionally  been  isolated  from  the 
cerebro-spinal  fluid  and  blood. 

(4)  Microscopic  Characters. — Clinically,  microscopic  investiga- 
tion is  probably  the  most  valuable  mode  of  examination  of  the 
cerebro-spinal  fluid. 

A  good  method  is  to  centrifuge  a  given  quantity  of  the  fluid,  say 
5  c.c.  for  five  minutes,  thereby  collecting  into  a  small  deposit  all  the 
cellular  elements  which  may  be  present.  We  then  carefully  decant 
off  all  the  superjacent  fluid,  turn  the  empty  tube  upside  down  and  scrape 
the  bottom  with  a  fine,  newly-made  capillary  pipette.  In  this  way  we 
collect  the  sediment,  which  is  transferred  to  a  slide,  fixed  by  heat 
or  alcohol-ether,  stained  by  methyl  blue  or  by  Jenner's  stain,  mounted 
in  Canada  balsam  and  examined  with  the  microscope. 

Specimens  prepared  as  above  described  afford  a  permanent  record 
of  the  variety  and  intensity  of  the  cellular  contents  present.  To  obtain 
absolute  accuracy  of  counting  we  employ  Fuchs  and  Rosenthal's  ^ 
counting-chamber,  a  modification  of  the  Zeiss  blood-counting  chamber. 
In  using  this,  a  small  quantity  (10  cubic  mm.)  of  cerebro-spinal  fluid 
is  mixed  by  means  of  a  special  pipette  with  1  cubic  mm.  of  a  staining 
fluid  containing  methyl  violet  and  acetic  acid.  A  drop  of  the  mixture 
is  placed  on  the  counting  stage,  and  the  cells  are  counted.  The  results 
so  obtained  correspond  with  those  found  in  centrifuged  deposits,  but 
are  more  accurate.  But  the  preparation  so  obtained  is  not  a  per- 
manent one,  and  I  am,  therefore,  now  in  the  habit  of  employing  both 
the  centrifuge  and  the  counting  chamber — the  one  to  yield  a  per- 
manent specimen,  the  other  to  ensure  accurate  counting  of  the  cellular 
contents  of  the  fluid. 

In  rare  cases  we  may  find  parasites.  Thus,  for  example, 
Castellani  and  Bruce  ^  found  the  trypanosome  of  sleeping-sickness 
not  only  in  the  blood  of  such  patients  but  also  in  the  cerebro- 

^   Wiener  medizini&che  Presse,  1904,  s.  2084. 
2  Brit.  Med.  Journ.,  November  21,  1903. 


440  NERVOUS    DISEASES 

spinal  fluid,  where  it  is  accompanied  by  lymphocytosis.  In  fact, 
it  is  easier  to  identify  the  trypanosome  in  the  cerebro-spinal  fluid 
than  in  the  blood,  wherein  it  is  likely  to  be  obscured  by  blood  cor- 
puscles. In  a  few  cases  of  metastatic  malignant  growths  of  the 
spinal  cord  or  of  its  meninges,  tumour-cells  have  been  found  in 
the  fluid.  But  this  is  inconstant,  though  tumour-cells,  if  present, 
have  a  high  positive  diagnostic  value. 

By  far  the  most  valuable  point  to  be  determined  microscopically 
is  the  presence  or  absence  of  leucocytes,  observing  not  only  their 
number  but  their  type.     This  is  the  so-called  cyto-diagnosis. 

Normal  cerebro-spinal  fluid  contains  no  polymorpho-nuclear 
leucocytes  and  only  an  occasional  small  mono-nucleated  lymphocyte, 
with  now  and  then  a  few  endothelial  plates.  Examination  of  the 
centrifuged  deposit  with  a  magnification  of  400  diameters,  accord- 
ing to  the  technique  described,  should  show  an  average  of  not  more 
than  two  or  three  lymphocytes  to  the  field,  or  from  1  to  3  per 
cubic  mm.  Sometimes  we  find  no  cells  of  any  sort.  But  in 
certain  organic  diseases  of  the  central  nervous  system  or  its  mem- 
branes, there  may  be  a  pleocytosis  or  excess  of  leucocytes — ^poly- 
morphs or  monomorphs.  Briefly  stated,  in  cases  of  acute  microbic 
infection  of  the  brain  and  meninges,  especially  the  suppurative 
varieties,  we  find  a  polynuclear  pleocytosis,  where  the  leucocytes 
are  mostly  polymorphs,  with  some  large  monomorphs  as  well. 
But  it  is  the  acuteness  of  the  inflammatory  process,  not  its  microbic 
origin,  which  is  the  chief  factor  in  producing  polynuclear  pleo- 
cytosis. Thus  I  have  experimentally  produced  abundant  poly- 
nuclear pleocytosis  in  monkeys  by  injecting  sterile  salt  solution 
or  a  sterile  emulsion  of  coloured  particles  into  the  spinal 
theca. 

When  recovery  begins,  in  acute  meningitis,  the  polynuclear 
leucocytes  in  the  cerebro-spinal  fluid  diminish  in  numbers  and 
become  replaced  by  lymphocytes.  These  latter  in  turn  disappear 
as  convalescence  becomes  complete. 

If  a  brain  abscess  be  present  without  impHcation  of  the 
superjacent  meninges,  as  sometimes  occurs,  the  cerebro-spinal  fluid 
shows  no  excess  of  leucocytes.  Examination  of  the  fluid  is  there- 
fore a  valuable  means  of  distinguishing  between  meningitis  and 
brain  abscess.  In  both  conditions  a  blood-count  shows  a  great 
excess  of  polymorphs  in  the  blood  :  these  may  number  from 
10,000  to  25,000  or  more  (instead  of  from  8000  to  10,000  per  cubic 


THE    CEREBRO-SPINAL    FLUID  441 

millimetre  as  in  health),  the  leucocytosis  of  the  blood  being,  as  a 
rule,  higher  in  meningitis  than  in  brain  abscess. 

But  in  subacute  and  chronic  affections  of  the  meninges,  whether 
tuberculous,  syphilitic,  or  from  other  causes,  e.g.  lead-encephalo- 
pathy,  also  in  certain  chronic  degenerative  diseases  of  the  central 
nervous  system,  we  usually  find  a  lymphocytosis,  i.e.  an  excess 
of  small  monomorphs,  sometimes  accompanied  by  a  small  pro- 
portion of  large  monomorphs.  In  cases  of  acutely  advancing  tuber- 
culous meningitis  we  often  find  a  considerable  proportion  of  poly- 
morphs (30  per  cent,  and  upwards)  amongst  the  monomorphs. 
There  is  often  a  marked  lymphocytosis  in  cases  of  mumps,  also 
during  an  attack  of  herpes  zoster  and  for  a  number  of  days  after- 
wards. 

In  the  early  days  of  an  attack  of  acute  anterior  pohomyelitis, 
before  the  onset  of  paralytic  symptoms,  we  find  well-marked 
changes  in  the  cerebro-spinal  fluid,  consisting  in  a  mixed  pleocytosis 
(chiefly  monomorphs,  with  some  polymorphs),  together  with  an 
excess  of  globuHn.  Meanwhile  the  blood  also  shows  a  distinct 
leucocytosis,  with  a  relatively  high  proportion  of  monomorphs. ^ 
In  cases  of  acute  chorea  we  occasionally  find  a  mixed  pleocytosis, 
proving  that  this  disease  is  no  longer  to  be  classed  as  a  pure  neurosis. 

In  several  cases  of  lymphatic  leuksemia,  at  the  Westminster 
Hospital,  and  in  a  case  of  chloroma,  Hebb  has  also  observed  marked 
lymphocytosis  of  the  cerebro-spinal  fluid. 

In  functional  nervous  diseases  the  fluid  is  normal. 

Let  us  study  some  illustrative  cases.  One  case  was  an  example 
of  epidemic  cerebro-spinal  meningitis,  in  a  patient  who  was  comatose 
and  apparently  moribund.  The  cerebro-spinal  fluid  was  under 
excessive  pressure,  of  turbid  appearance,  and  the  centrifuged 
deposit  showed  microscopically  an  average  of  87*3  polymorphs  to 
the  field.  Within  many  of  the  leucocytes  the  meningo -coccus  was 
readily  distinguished.  The  withdrawal  of  about  an  ounce  of  fluid 
caused  marked  improvement  in  the  symptoms  and  the  patient 
made  a  good  recovery.  Another  case  was  that  of  an  officer  who 
had  chronic  otitis  media  on  the  left  side.  He  rapidly  developed 
mental  dulness  and  slight  aphasic  symptoms,  with  some  fever.  In 
his  case  the  fluid  was  turbid,  and  showed  no  fewer  than  371  poly- 
morphs to  the  field.  Operation  was  at  once  undertaken  and  an 
inflamed  area  of  brain  tissue  in  the  temporal  lobe  was  exposed. 

^  Fressell,  Journal  of  American  Med.  Assoc,  March  4,  1911. 


442  NERVOUS    DISEASES 

No  abscess  was  found.      The  symptoms  rapidly  subsided  and  the 
patient  made  a  complete  recovery. 

As  an  instance  in  which  the  cerebro -spinal  fluid  was  normal  may 
be  mentioned  the  case  of  a  child,  in  whom,  as  is  so  often  the 
case,  a  deep-seated  pneumonia  was  ushered  in  by  head  symp- 
toms simulating  meningitis — so-called  "  meningism."  There  were 
marked  headache,  some  head-retraction,  and  squint.  Moreover, 
an  older  child  in  the  same  family  had  previously  died  from  tuber- 
culous meningitis,  and  the  parents  were  therefore  in  considerable 
anxiety  as  to  the  possibiUty  of  this  case  being  another  of  the  same 
nature.  The  cerebro-spinal  fluid,  however,  showed  no  excess  of 
cells,  and  Kernig's  sign  was  absent.  Meningitis  was  therefore  less 
likely  than  a  transient  toxic  meningism,  and  an  encouraging  prog- 
nosis was  given,  which  proved  correct.  Meningism  occurs  chiefly 
in  children,  and  especially  in  those  with  a  tuberculous  diathesis. 
The  symptoms  appear  during  the  course  of  some  other  acute 
febrile  illness.  After  the  meningitic  symptoms  have  subsided 
there  is  often  a  stage  of  transient  cerebellar  ataxia,  which  also 
ultimately  clears  up.^ 

With  regard  to  cases  of  lymphocytosis,  the  most  striking  results 
are  those  observed  in  parenchymatous  cerebro-spinal  syphihs, 
which  includes  general  paralysis  of  the  insane,  tabes  dorsalis,  and 
"  optic  tabes."  The  lymphocytosis  in  these  affections  (which  are 
essentially  the  same  disease  etiologically,  and  which  clinically  are 
not  infrequently  combined  in  the  same  patient)  is  more  marked 
than  in  any  other  form  of  organic  nervous  disease.  Thus  in  a 
series  of  forty  cases  of  general  paralysis  examined  by  me,  the 
average  number  of  lymphocytes  was  98.7  per  cubic  mm.,  the  lowest 
count  in  any  one  case  being  34.4,  and  the  highest  462.  In  a  series 
of  twenty-two  tabetics,  the  lowest  count  was  19.2,  the  highest 
477"  1,  and  the  average  number  per  cubic  mm.  for  the  whole  series 
was  144-3. 

A  point  of  importance  noticed  in  cases  of  tabes  and  general 
paralysis  is  that  not  only  is  lymphocytosis  present  in  practically 
every  case,  but  it  is  often  extremely  marked  when  the  other 
symptoms  of  the  disease  are  very  slight.  Thus,  for  example,  one 
patient  had  Ughtning-pains,  analgesia  of  the  tendo  AchilHs,  but  no 
ataxia,  no  abnormality  of  the  pupils,  and  brisk  knee-  and  ankle- 
jerks.   Yet  his  cerebro-spinal  fluid  showed  150  lymphocytes  per  cubic 

1  Foerster,  Neurolog.  Centralhlatt,  1913,  p.  1414. 


THE    CERERRO-SPINAL    FLUID  443 

millimetre,  and  his  was  undoubtedly  an  early  case  of  tabes.  The 
same  applies  to  general  paralysis.  One  patient  with  239'6  lympho- 
cytes per  cubic  mm.  was  an  early  case,  with  practically  no  mental 
symptoms,  simply  a  slight  loss  of  memory  and  a  history  of  two 
attacks  of  unconsciousness  followed  by  transient  aphasia  and 
weakness  of  the  right  hand — •"  congestive  attacks." 

In  general  paralysis  the  fluid  practically  always  contains 
"  plasma  cells."  These  are  mononuclear  cells,  somewhat  larger 
than  the  ordinary  lymphocytes,  with  an  eccentrically-placed  circular 
nucleus  which  has  a  characteristic  "  clock-face  "  arrangement  of 
its  chromatin  granules.  The  surrounding  protoplasm  is  abundant 
and  stains  deep  pink  with  the  pyronin  methyl-green  stain.  ^ 

We  therefore  possess  in  the  cytological  examination  of  the 
cerebro-spinal  fluid  a  valuable  means  of  recognising  tabes  and 
general  paralysis  in  their  earliest  stages.  If  no  excess  of  lymphocytes 
be  present,  these  two  varieties  of  parenchymatous  or  cerebral  syphilis 
can  usually  be  excluded."^  Another  point  of  interest  is  that  during 
the  pyrexial  attacks  of  general  paralysis,  there  is  a  temporary 
polynuclear  pleocytosis,  not  only  of  the  blood  but  of  the  cerebro- 
spinal fluid.  Thus  in  a  case  of  my  own  there  were  118  polymorphs 
and  25  monomorphs  per  cubic  mm.  Pappenheim  ^  has  also  recorded 
similar  cases. 

Another  point  of  importance  is  that  syphihs  by  itself,  unless 
there  be  an  active  syphihtic  lesion  of  the  central  nervous  system, 
or  its  meninges,  as  in  the  well-known  syphilitic  headache,  produces 
Httle  or  no  excess  of  cells  in  the  cerebro-spinal  fluid.  A  transient 
lymphocytosis  may,  however,  occur  during  the  secondary  eruption 
of  syphihs,  not  only  in  patients  with  symptoms  of  headache,  in- 
somnia, &c.,  but  also,  though  less  frequently,  in  patients  without 
any  symptoms  pointing  to  cerebral  nervous  disease.     In  tertiary 

^  Rehm,  Histol.  u  histofdth,  Arbeit  uber  die  Grosshirnrinde,  Bd.  3,  Sept. 
2,  1909. 

Henderson  and  Winifred  Muirhead,  Eev.  of  Neurol,  ani  Psychiat.,  1913, 
p.  195. 

^  This  rule,  however,  is  not  without  exceptions,  for  I  have  seen  a  case  of 
tabes,  with  ataxia,  Argyll-Robertson  pupils,  and  absent  knee-  and  ankle-jerks, 
in  which  the  cerebro-spinal  fluid  contained  only  3"3  lymphocytes  per  mm', 
and  another  advanced  case  with  only  4  lymphocytes  per  mm'  and  a  negative 
Wassermann  reaction.  Erb,*  Head  and  Fearnsides,t  and  others,  have  also 
recorded  similar  cases,  which  signify  that  the  disease  is  no  longer  progressive 
but  is  in  a  quiescent  stage,  either  spontaneously  or  as  a  result  of  treatment. 

'  Monatschrift  fiir  Psychiatrie  und  Neurologie,  1907,  s,  536. 

*  Deutsche  Zeltsch.  f.  Nervenheilkunde,  1907,  p.  438. 
t  Brain,  1914,  vol.  37,  p.  101. 


444  NEEVOUS    DISEASES 

syphilis  again,  without  nervous  phenomena,  the  cerebro-spinal 
fluid  is  usually  normal. 

Thus  we  see  that  the  presence  in  the  cerebro-spinal  fluid  of  a 
large  lymphocytosis  with  a  positive  Wassermann  reaction,  and  the 
presence  of  globulin,  in  a  patient  who  has  had  syphilis,  is  of  grave 
significance  and  indicates  cerebro-spinal  syphilis,  either  of  the 
meningo -vascular  type  or  of  the  parenchymatous  type,  as  in  tabes 
or  general  paralysis.  In  such  cases  we  should  carefully  examine 
for  other  signs  of  organic  disease,  especially  for  Argyll-Robertson 
pupils,  early  optic  atrophy,  alterations  in  the  reflexes,  and  sensory 
changes.  Even  if  no  clinical  sign  of  organic  disease  be  present, 
the  presence  of  globulin,  lymphocytosis,  and  a  positive  Wasser- 
mann reaction  in  the  cerebro-spinal  fluid  is  an  indication  for 
energetic  anti -specific  treatment,  in  the  hope  of  preventing 
further  developments. 

The  presence  of  lymphocytosis  in  tuberculous  meningitis  is 
readily  understood,  also  that  which  occurs  in  tuberculous  tumours 
on  the  surface  of  the  brain.  It  is  more  difficult  at  present  to 
account  for  the  occasional  excess  of  lymphocytes  in  cerebral 
neoplasms.  Thus  one  case  of  glioma  of  the  centrum  ovale  had  no 
fewer  than  75  lymphocytes  to  the  field,  a  count  which  led  one 
to  expect  a  tuberculous  mass,  there  being  no  possibility  of  syphilis. 
Yet  the  autopsy  showed  a  glioma  which  had  in  no  way 
approached  the  meninges  ;  and  a  haemorrhage  into  the  substance 
of  the  tumour  had  caused  death  by  bursting  into  the  lateral 
ventricle. 

The  occurrence  of  eosinophile  cells  in  the  cerebro-spinal  fluid 
is  practically  pathognomonic  of  cysticercus  infection  of  the  brain 
or  spinal  cord. 

Therapeutic  Applications  of  Thecal  Puncture. — ^Lumbar 
puncture  was  originally  introduced  by  Quincke  for  the  purpose 
of  relieving  intra-cranial  pressure  in  tuberculous  meningitis.  This 
it  does  for  the  time,  though  it  is  more  often  palliative  than  curative. 
In  one  case  of  mine  the  patient,  a  young  man,  comatose  and 
apparently  moribund,  regained  consciousness  for  a  day,  after  the 
withdrawal  of  22  c.c.  of  cerebro-spinal  fluid.  The  fluid  was  allowed 
to  flow  until  the  increased  intra -thecal  pressure  fell  to  normal. 
The  importance  of  this  procedure,  not  only  from  sentimental 
reasons  but  possibly  on  medico-legal  grounds,  is  obvious.  In 
any  case  we    can    usually  diminish    or  abolish  the    convulsions 


THE    CEREBRO-SPINAL    FLUID  445 

which  are  so  distressing  to  the  onlookers.  But  sometimes 
lumbar  puncture  has  proved  curative,  even  in  tuberculous 
meningitis.  Thus  in  cases  recorded  by  Freyhan/  Henkel,^ 
Barth,^  Pitfield  ^  and  others,  tubercle  bacilli  were  demonstrated 
in  the  cerebro -spinal  fluid  and  yet  the  patients  ultimately  recovered, 
after  repeated  punctures. 

In  other  forms  of  meningitis,  associated  with  a  polynuclear 
pleocytosis  (apart  from  infective  cases  secondary  to  bone  disease), 
especially  in  epidemic  cerebro-spinal  meningitis,  good  results  have 
been  obtained  by  the  injection  of  antiseptic  substances,  after  with- 
drawal of  a  corresponding  quantity  of  cerebro-spinal  fluid.  For 
this  purpose,  a  1  per  cent,  solution  of  lysol  has  been  found  useful, 
10  cubic  centimetres  being  introduced  at  each  sitting.  Flexner's 
serum,  prepared  from  immunised  horses,  injected  in  doses  of 
about  30  c.c.  repeated  on  several  successive  days,  has  also  had 
highly  encouraging  results.^ 

Other  sera  are  also  introduced  intra-thecally.  Thus  in  cerebro- 
spinal syphilitic  diseases,  including  tabes  and  general  paralysis, 
we  may  employ  the  patient's  own  blood-serum,  diluted  and 
sterilised,  after  a  previous  intra-venous  injection  of  salvarsan  or 
neo-salvarsan.  Again,  in  the  acute  febrile  stage  of  poliomyelitis 
anterior  acuta,  a  curative  serum  can  be  injected  intra-thecally. 

In  delirium  tremens  a  rapid  sedative  action  can  be  obtained 
by  the  intra-thecal  injection  of  50  cubic  centimetres  of  a  1  per  cent, 
solution  of  sodium  bromide,  after  previous  withdrawal  of  an  equiva- 
lent amount  of  cerebro-spinal  fluid.^ 

In  intra-cranial  pressure  due  to  other  causes,  as,  for  example, 
in  inoperable  or  inaccessible  cerebral  tumours,  lumbar  puncture  is 
sometimes  of  distinct  benefit  as  a  palliative  measure,  by  diminishing 
urgent  pressure  and  thereby  relieving  headache,  vertigo,  and  other 
symptoms.  Hitherto  to  relieve  intra-cranial  pressure  and  to 
diminish  optic  neuritis  it  has  been  the  custom  to  trephine  the 
skull  as  a  palliative  measure.  But  lumbar  puncture  is  quicker, 
simpler,  and  less  dangerous  than  a  major  cranial  operation.-  I  per- 
formed it  in  three  cases  of  intra-cranial  tumour.     In  all  of  them  the 

1  Deutsche  medizinische  Wochenschrift,  1904,  No.  36. 

2  Miinchener  medizinische  Wochenschrift,  1900,  s.  133. 

3  Ibid.,  1902.  No.  21. 

*  American  Journal  of  Medical  Sciences,  July  1913,  p.  37. 

5  Ker,  Edin.  Med.  Journal,  Oct.  1908. 

^  Kramer,  Boston  Med.  and  Surg.  Journ.,  Oct.  1913,  p.  646. 


446  NERVOUS    DISEASES 

headache  and  vertigo  were  greatly  relieved  for  several  weeks  after 
the  puncture,  and  an  opportunity  was  afforded  of  studying  the 
patient's  focal  symptoms  with  a  view  to  subsequent  removal  of  the 
growth.  In  intra-cranial  growths  we  must  be  careful  not  to 
withdraw  too  large  a  quantity  of  cerebro-spinal  fluid,  lest  sudden 
diminution  of  pressure  cause  a  haemorrhage  into  the  tumour  (a 
result,  by  the  way,  which  sometimes  occurs  after  a  palliative 
trephining).  In  fractures  of  the  base  of  the  skull,  coma  may  be 
quickly  relieved  by  the  withdrawal  of  cerebro-spinal  fluid.  I  saw 
such  a  patient,  after  a  carriage  accident,  in  whom  lumbar  puncture 
was  followed  by  rapid  improvement.  The  procedure  may,  if 
necessary,  be  repeated  several  times  on  successive  days. 

In  cases  of  coma  due  to  sunstroke,  withdrawal  of  cerebro-spinal 
fluid  often  has  an  almost  immediate  curative  effect.  The  fluid 
in  such  cases  is  usually  under  increased  pressure  and  shows  a  poly- 
morph pleocytosis,  indicative  of  an  acute  meningeal  reaction. 

Uraemic  coma  and  convulsions,  and  attacks  of  puerperal  eclamp- 
sia, are  often  relieved  in  a  striking  manner  by  lumbar  puncture,  and 
in  several  instances  life  has  undoubtedly  been  saved  by  such  means. 
For  example,  McVail  ^  records  two  cases  of  acute  nephritis  in  which, 
notwithstanding  energetic  treatment  by  purgatives,  hot-air  baths 
and  pilocarpin  to  induce  free  perspiration,  coma  and  convulsions 
supervened.  Lumbar  puncture  was  performed,  20  to  28  c,c.  of 
cerebro-spinal  fluid  were  withdrawn,  and  within  three  or  four 
hours  the  coma  passed  of!,  the  convulsions  ceased,  and  both  patients 
ultimately  made  a  complete  recovery.  Cases  like  these  raise  the 
question  as  to  whether  the  headache,  coma,  and  convulsions  in 
nephritis  are  really  caused  entirely  by  "  ursemic  poisoning  "  of  the 
brain-centres,  or  whether  they  may  not  be  largely  due  to  a  sudden 
increase  of  intra-cranial  pressure  as  part  of  the  general  oedema. 

Again,  in  cases  of  tetanus,  we  know  that  the  tetanus  poison 
has  a  selective  action  on  the  motor  nerve-cells  of  the  spinal  cord 
and  brain.  Therefore,  in  addition  to  removing  the  tetanus 
bacilli  at  the  site  of  inoculation,  by  excision  of  the  original  wound, 
we  endeavour  to  neutralise  the  toxin  by  means  of  antitoxin. 
This  is  sometimes  administered  hypodermically,  or  better,  intra- 
venously, but  only  a  fraction  of  the  antitoxin  thus  injected  reaches 
the  nervous  system,  the  main  mass  being  distributed  uselessly  to 
other  tissues.     It  is  more  efficacious,  as  Roux  and  others  have 

'    Brit.  Med,  Journ.,  1903,  vol.  ii. 


THE    CEREBRO-SPINAL    FLUID  447 

shown,  if  injected  into  the  cranial  cavity  through  a  small  trephine 
opening,  and  some  remarkable  recoveries  have  followed  this  method 
of  treatment.  But  the  procedure  is  not  free  from  danger.  In  one 
case  at  least,  ^  a  patient  died  of  cerebral  abscess  at  the  site  of  the 
trephine-opening  eight  weeks  afterwards,  long  after  all  symptoms 
of  tetanus  had  disappeared.  It  is  simpler  and  still  better  to 
administer  the  antitoxin  (with  perhaps  the  addition  of  stovaine) 
by  means  of  lumbar  puncture.  Strychnine  poisoning  is  also  suc- 
cessfully treated  by  intra-thecal  administration  of  eucaine.  It 
may  be  necessary  to  give  a  general  anaesthetic,  to  relax  the 
opisthotonos,  before  performing  the  spinal  puncture. 

Injection  of  anaesthetic  drugs  by  thecal  puncture — so-called 
spinal  anaesthesia — is  useful  when  we  desire  to  perform  operations 
on  the  lower  limbs  or  trunk  without  rendering  the  patient's  brain 
unconscious.  Various  substances  have  been  successfully  employed 
as  spinal  anaesthetics,  amongst  which  may  be  mentioned  magnesium 
sulphate,  cocaine,  stovaine,  and  a  mixture  of  novocaine  with 
strychnine.-  It  is  desirable,  if  possible,  to  have  a  solution  which  is 
isotonic  with  the  blood-serum,  i.e.  having  the  same  osmotic  tension. 

For  spinal  anaesthesia  in  operations  on  the  pelvis  and  lower 
limbs  we  generally  select  the  first  or  second  lumbar  interspace, 
whilst  Jonnesco  prefers  "  dorso-lumbar "  injection  between  the 
twelfth  thoracic  and  the  first  lumbar  vertebra,  thereby  producing 
analgesia  of  the  whole  abdomen  and  lower  limbs.  We  perform 
our  puncture  in  the  mesial  line,  so  that  the  roots  of  both  sides 
may  be  equally  affected.  Before  injecting  the  ansesthetising 
solution,  we  withdraw  a  quantity  of  cerebro-spinal  fluid,  ex- 
ceeding in  amount  the  fluid  to  be  introduced. 

Spinal   anaesthesia   is   essentially   a   root   anaesthesia,    due   to 

1  Gibbs,  Brit.  Med.  Journ.,  July  1,  1899. 

2  The  following  are  examples  of  anaesthetising  solutions : — 

1.  Stovaine,  5  per  cent. ;  glucose,  5  per  cent,  in  water.  Sp.  gr.  =  1023. 
Dose=l  CO.     (Barker,  Brit.  Med.  Journ.,  1908,  p.  248.) 

2.  Stovaine,  4  per  cent.;  sod.  chloride,  0*11  per  cent.:  suprarenin 
borate,  0"01  per  cent,  in  water.  Sp.  gr.  =  I00o.  Dose  =  l  c.c.  (Bier, 
quoted  by  Barker,  Brit.  Med.  Journ.,  1907,  p.  665.) 

3.  Stovaine,  1-5  per  cent. ;  cocaine,  0*5  percent,  in  water.  Dose  =  4  c.c. 
(Chaput,  La  Presse  Medicate,  1907,  p.  753.) 

4.  Novocaine,  2  per  cent. ;  suprarenin  borate,  0"009  per  cent. ;  NaCl, 
0'9  per  cent.  Sp.  gr.  =  1014.  Dose  =  5  c.c.  (Braun,  Deutsche  med. 
Wochenschrift,  1905,  s.  1667.) 

5.  Strychnine  sulphate,  5  to  10  eg. ;  sterilised  water,  100  grams.  Of 
this  solution  1  c.c.  is  mixed  with  3  to  10  eg.  of  stovaine,  and 
the  mixture  is  injected.  (Jonnesco,  Brit.  Med.  Journal.  1909, 
p.  1396.) 


448  NERVOUS    DISEASES 

paralysis  of  the  posterior  roots.  On  injecting  a  solution  of 
stovaine  in  the  lumbar  region,  the  earliest  objective  signs  are 
disappearance  of  the  knee-jerks  (usually  within  one  minute),  then 
of  the  ankle -jerks  (within  two  or  three  minutes),  the  superficial 
reflexes  remaining  as  yet  unchanged.  Concurrently  with  the 
abolition  of  the  deep  reflexes  there  occurs  slight  analgesia  of  the 
perineum  and  genitals,  without  loss  of  tactile  sensibility.  The 
analgesia  gradually  deepens  and  spreads  over  the  lower  limbs,  and 
after  four  or  five  minutes  the  plantar  and  cremasteric  reflexes 
disappear.  Temperature -sense  becomes  lost.  Tactile  and  pressure- 
sense  disappear  much  later  and  may  be  preserved  throughout. 
Sense  of  position  is  last  and  least  affected.  The  dartos  or  scrotal 
reflex  is  unaffected.  Motor  paralysis,  due  to  affection  of  the 
anterior  roots,  supervenes  last  of  all,  in  five  or  six  minutes, 
beginning  in  the  feet  and  soon  affecting  the  whole  musculature  of 
the  lower  limbs.  The  deep  structures  also  become  analgesic.  If  it 
is  desired  to  reach  the  higher  roots  by  a  heavy  anaesthetising  fluid, 
it  is  advisable  to  elevate  the  pelvis  higher  than  the  thorax,  to 
permit  the  fluid  to  gravitate  towards  the  thoracic  region.  In  this 
way  the  anaesthesia  may  extend  as  high  as  the  nipples,  or  even  to 
the  upper  limbs.  If  the  injection  be  made  with  the  patient  lying 
on  his  side,  the  heavy  anaesthetising  solution  gravitates  to  the 
dependent  side  and  therefore  exercises  its  effects  chiefly,  and  it 
may  be  entirely,  on  the  roots  of  that  side.  Thus,  for  example, 
by  laying  a  patient  on  his  left  side  and  injecting  in  that  posture 
Barker  ^  was  able  to  amputate  the  left  leg  painlessly,  without 
producing  sensory  or  motor  impairment  of  the  right  lower 
limb. 

After  lasting  for  45  to  90  minutes,  the  paralytic  phenomena 
begin  to  pass  off.  First  motor  power  returns,  then  the  analgesia 
fades  away,  and  last  of  all,  the  reflexes,  superficial  a,nd  deep, 
reappear. 

Spinal  anaesthesia  by  means  of  stovaine  can  also  be  employed,  as 
Jonnesco  ^  has  shown,  at  higher  levels  of  the  cord  if  strychnine  be 
added  to  the  stovaine  so  as  to  protect  the  cord  from  depressing  vaso- 
motor or  respiratory  effects.  For  operations  on  the  head,  neck,  and 
upper  limbs  Jonnesco  recommends  an  "upper  dorsal"  puncture, 
between  the  first  and  second  dorsal  vertebrae.     Injections  at  any  higher 

1  Brit.  Med.  Journ..  1908,  p.  246. 

2  Ibid.,   1909,  p.  1398. 


THE    CEREBRO-SPINAL    FLUID 


449 


level  are  unnecessary,  besides  being  too  close  to  the  medulla  oblongata 
for  safety.  For  operations  on  the  abdomen  and  lower  limbs,  Jonnesco 
recommends  a  "  dorso-lumbar  "  injection  between  the  twelfth  dorsal 
and  fifth  lumbar  vertebrte  (see  Fig.  224).  It  should  be  borne  in  mind 
that  both  in  "  upper  dorsal  "  and  in  "  dorso-lumbar  "  punctures  the 
spinal  cord,  lies  immediately  subjacent  to  the  site  of  the  puncture,  and 
it  is  therefore  important  to  stop  the  needle  inmediately  its  point  has 
penetrated  within  the  spinal  theca,  so  as  to  avoid  injury  to  the  sjDinal 
cord. 

In  performing  an  "upper  dorsal"  injection  we  first  feel  for  the 


1-2  D. 


Fig.  224. 


-Showing  sites  of  "  upper  dorsal  "  and  of  "  dorso-lumbar  ' 
injections  for  spinal  anaesthesia.     (Jonnesco.) 


vertebra  prominens  (seventh  cervical).  Then  taking  the  first  dorsal 
spine  immediately  below  this  (the  patient's  head  being  strongly  flexed, 
so  as  to  separate  the  laminEs),  we  slowly  push  in  our  needle,  in  the  mesial 
plane,  along  the  upper  border  of  the  second  dorsal  spine.  On  reaching 
the  dura  mater  a  momentary  resistance  is  felt,  and  when  the  needle 
reaches  the  arachnoidal  space,  cerebro-spinal  fluid  at  once  begins  to 
trickle.  Unless  fluid  is  seen  to  escape,  we  cannot  be  sure  that  the 
point  of  the  needle  is  in  the  arachnoidal  cavity.  Sometimes  it  is  useful 
to  make  the  patient  cough,  to  start  the  fluid.  As  soon  as  the  fluid 
begins  to  escape  w^e  attach  our  injection-syringe  and  slowly  introduce 
the  mixture  of  stovaine  and  strychnine.  After  an  upper  dorsal  in- 
jection, if  the  operation  is  to  be  on  the  head  or  neck,  the  patient  should 

2f 


450  NERVOUS   DISEASES 

be  on  his  back.     If  the  operation  is  to  be  on  the  upper  limbs  or  thorax, 
he  should  sit  up  for  two  or  three  minutes  before  lying  down. 

For  upper  dorsal  injections  Jonnesco  recommends  relatively  smaller 
amounts  of  strychnine  (J  mg.)  and  of  stovaine  (1  to  3  eg.),  whereas 
in  dorso-lumbar  injections  the  doses  of  strychnine  (1  mg.)  and  of 
stovaine  (4  to  10  eg.)  are  large. 

Spinal  anaesthesia  is  contra -indicated  in  severe  scoliosis,  because 
of  the  difficulty  in  accurately  penetrating  the  theca.  It  is  also 
better  avoided  in  young  children  and  in  most  cases  of  hysteria. 
Even  apart  from  such  cases,  it  should,  I  believe,  be  reserved  for 
very  special  conditions,  as,  for  example,  acute  abdominal  cases, 
conditions  of  shock,  and  severe  cardiac  or  pulmonary  diseases 
where  a  general  anaesthetic  is  particularly  dangerous.  From  the 
patient's  point  of  view,  complete  unconsciousness  is  generally 
preferable  to  the  mental  strain  of  remaining  conscious  whilst  an 
operation  is  being  performed  on  his  analgesic  legs  or  trunk. 

Of  the  morbid  phenomena  which  sometimes  follow  spinal 
anaesthesia,  the  most  frequent  is  headache  ;  this  is  often  of  great 
severity  and  may  last  for  days  ;  it  is  probably  due  to  the  altered 
intra -cranial  pressure  produced  by  the  addition  of  the  anaesthetising 
solution,  and  may  generally  be  relieved  by  a  simple  lumbar  puncture, 
withdrawing  from  10  to  20  c.c.  of  fluid.  In  three-fourths  of  cases 
of  spinal  anaesthesia,  according  to  Schwarz,^  there  is  a  slight  transient 
albuminuria,  lasting  for  a  week  or  more.  Another  sequela,  fortu- 
nately an  uncommon  one,  is  ocular  palsy,  chiefly  of  one  external 
rectus  but  sometimes  of  some  other  ocular  muscle  ;  such  palsy 
may  last  for  days  or  weeks,  but  ultimately  clears  up. 

^  Zeitschrift  fiir  Chirurgie,  1907,  s.  651. 


CHAPTER   XXIV 

DISORDERS    OF    SLEEP 

"  The  innocent  sleep. 
Sleep  that  knits  up  the  ravelled  sleeve  of  care, 
The  death  of  each  day's  life,  sore  labour's  bath, 
Balm  of  hurt  minds,  great  nature's  second  course, 
Chief  nourisher  in  life's  feast." 

— Shakespeabe,  Macbeth. 

Most  of  us  spend  about  one-third  of  our  life  asleep.  Neverthe- 
less the  physiology  of  sleep  is  not  yet  completely  understood.  Let 
us  recall  the  chief  phenomena  of  ordinary  healthy  sleep.  Firstly, 
there  is  diminution  and  then  loss  of  conscious  recognition  of  ordi- 
nary stimuli,  such  as  would  ordinarily  attract  our  attention, 
whether  these  stimuli  be  derived  from  the  outer  world  or  from 
within  the  sleeper's  own  organism.  There  is  also,  as  consciousness 
is  becoming  blunted,  a  characteristic  and  indescribable  sense  of 
well-being.  Voluntary  movements  become  languid  and  ultimately 
cease,  and  the  muscles  of  the  limbs  relax.  Meanwhile  there 
develops  double  ptosis  or  drooping  of  the  eyelids  ;  the  pupils  con- 
tract ;  the  respiratory  movements  become  slower  and  deeper,  the 
pulse  is  slowed,  the  cutaneous  vessels  dilate  to  a  slight  extent  and 
the  general  temperature  of  the  body  falls,  whilst  many  processes  of 
metabolism,  such  as  those  of  digestion  and  of  certain  secretions, 
are  retarded.  Many  of  the  phenomena,  e.g.  the  contracted  pupils, 
slow  pulse,  &c.,  are  evidences  of  increased  activity  of  the  auto- 
nomic system. 

Various  explanations  have  been  offered  to  account  for  all  these 
phenomena.  But  at  the  outset  we  should  recognise  that  the 
process  is  a  complex  one,  implicating  many  other  organs  besides 
the  brain.  An  animal  from  which  the  cerebral  hemispheres  have 
been  removed  still  shows  regular  alternations  of  sleep  and  waking. 

As  regards  the  condition  of  the  brain  during  natural  sleep,  it 
is  generally  admitted  that  it  is  anaemic.  If  we  observe  a  patient 
or  an  animal  that  has  been  trephined,  we  see  that  during  sleep 

451 


452  NERVOUS    DISEASES 

the  volume  of  the  brain  is  diminished  ;  it  sinks  in  and  becomes 
pale,  i.e.  the  cortical  vessels  are  contracted.  This  vaso-con- 
striction  is  not  confined  to  the  superficial  vessels  alone  ;  it  implicates 
the  whole  cerebral  circulation,  for  if  we  succeed  in  examining  the 
patient's  retinal  vessels  with  an  ophthalmoscope  without  wakening 
him,  we  find  that  they  present  a  similar  vaso-constriction.  Cerebral 
anaemia,  then,  is  one  important  factor  in  natural  sleep.  We  are 
all  familiar  with  the  difficulty  of  doing  mental  work  and  the  ten- 
dency to  fall  asleep  after  a  heavy  meal.  This  is  doubtless  ex- 
plained to  some  extent  by  the  occurrence  of  temporary  abdominal 
hypersemia  together  with  compensatory  cerebral  anaemia. 

Let  us  next  consider  the  condition  of  the  nerve-cells  during 
sleep.  The  activity  of  some  of  them,  certainly  of  the  cortical 
cells,  is  temporarily  diminished.  Some  writers  have  suggested 
that  this  is  due  to  a  retraction  of  the  dendrites,  by  a  sort  of  amoeboid 
movement  whereby  nerve-cells  previously  in  contact  become,  as  it 
were,  temporarily  insulated.  But  the  evidence  in  support  of  this 
theory  is  far  from  convincing.  In  fact,  modern  histological  obser- 
vation goes  to  show  that  nerve-cells  are  not  merely  in  contact 
but  that  neuro-fibrillse  are  continuous  from  cell  to  cell  throughout 
the  nervous  system. 

Other  writers  ascribe  the  phenomena  of  sleep  to  poisoning  of 
the  nerve-cells  by  accumulation  of  carbon  dioxide,  or  to  intoxication 
by  other  waste -products  of  metabolism  acting  as  narcotics.  Be  this 
as  it  may,  we  must  bear  in  mind,  as  Claparede  ^  has  urged,  that 
neither  carbon  dioxide  poisoning  nor  intoxication  is  a  necessary 
antecedent  to  sleep.  On  the  contrary,  we  usually  sleep  for  the  pur- 
pose of  avoiding  auto -intoxication  and  of  preventing  exhaustion,  not 
because  auto-intoxication  or  exhaustion  has  supervened.  Healthy 
sleep  is  not  necessarily  a  poisoning  of  certain  nerve-centres  by 
toxic  by-products.  We  may  feel  intensely  fatigued  without  being 
drowsy  and,  conversely,  we  may  feel  drowsy  without  being 
physically  or  mentally  fatigued.  Moreover  there  is  a  regular 
periodicity  whereby  a  healthy  person,  whether  fatigued  or  not, 
has  a  recurrent  appetite  for  sleep.  Sleep  has  a  constructive, 
anabolic,  invigorating  effect  on  the  whole  body.  Part  of  this 
effect  is  doubtless  due  to  physical  rest,  part  perhaps  to  inter- 
ruption in  the  production  of  toxins  arising  from  muscular  con- 

^  Archives  de  Biologie,  1905, 


DISORDERS    OF    SLEEP  453 

traction,  and  part  to  the  absence  of  stimuli  which  during  waking 
hours  excite  nervous  katabolism. 

Some  writers  have  assigned  special  importance  to  a  particular 
region  of  the  brain  in  connection  with  the  function  of  sleep,  and 
especially  to  the  floor  of  the  third  ventricle  and  the  Sylvian  aque- 
duct. In  support  of  this  they  point  out  the  familiar  ptosis  and 
the  tendency  to  divergent  strabismus,  both  of  which  might  be 
explained  as  due  to  paresis  of  the  ocular  nuclei.  They  also  recall 
the  well-established  fact  that  tumours  in  the  region  of  the  pituitary 
body  are  specially  likely  to  have  as  an  early  .symptom  persistent 
drowsiness  probably  from  sub-pituitarism.  Some  of  these  pheno- 
mena can  also  be  explained  as  due  to  cerebral  ana3mia,  the  tumour 
at  the  base  mechanically  compressing  and  narrowing  the  arteries 
which  form  the  circle  of  WilUs.  This  has  been  demonstrated  in 
several  instances,  notably  in  a  case  of  tumour  of  the  infundibulum 
and  floor  of  the  third  ventricle  recorded  by  Franceschi.^  I  myself 
had  under  my  care  a  similar  case  in  a  young  woman,  aged  twenty- 
six,  with  a  large  cystic  growth  of  the  pituitary  body  pressing 
upwards  on  the  floor  of  the  third  ventricle  (Figs.  225  and  225a),  in 
whom  the  chief  symptoms  were  paroxysms  of  overpowering  sleep. 
She  ultimately  passed  into  a  stuporose  condition  and  died.  No 
paralytic  phenomena  occurred  during  hfe,  nor  was  there  any  optic 
neuritis.^  Another  case  was  that  of  a  young  man  of  thirty-four 
who  had  intense  drowsiness,  paroxysmal  headaches,  and  signs  of 
dyspituitarism,  including  total  loss  of  sexual  power.  He  also  had 
blindness  of  the  right  eye  and  temporal  hemianopia  of  the  left, 
with  slight  pallor  of  the  right  optic  disc,  signs  pathognomonic  of 
a  lesion  of  the  optic  chiasma.  All  these  phenomena  were  due  to 
a  tumour  of  the  pituitary  body.  His  drowsiness  was  so  intense  that 
he  fell  asleep  if  he  sat  down,  and  only  with  difficulty  could  he  be 
roused  for  examination. 

Another  factor  in  the  production  of  natural  sleep  is  the  absence 
of  violent  external  stimuli  such  as  loud  sounds  or  dazzling  light ; 
therefore  silence  and  darkness,  by  withdrawal  of  stimuli,  conduce 
to  sleep.  The  pleasing  monotony  of  gently  reiterated  stimuli  often 
has  a  similar  soothing  effect  which  is  quite  sui  generis  and 
is  closely  analogous  to  the  condition  of  hypnosis.  It  cannot  be 
ascribed    to    cerebral  anaemia,  to    exhaustion,   nor   to    any  toxic 

action. 

^  Rivista  di  patologia  nervosa  e  nventale,  1904,  p.  457- 
^  Review  of  Neurology  and  Psychiatry,  1909,  p.  225. 


454 


NERVOUS    DISEASES 


We  recognise  difierent  degrees  of  normal  sleep,  according  to 
the  strength  of  stimulus  necessary  to  rouse  the  sleeper  to  a  con- 
sciousness  of   his   surroundings.      The  lightest   is   that   of   mere 


Fig.  225. 


Fig.  225A. 


Figs.    225   and   225a. — Cystic   tumour   of  pituitary    infundibulum,    containing 
colloid  material  and  compressing  the  third  ventricle  from  below  upwards. 

drowsiness,  a  stage  in  which  the  sleeper,  though  not  directing 
his  conscious  attention  to  surrounding  objects,  can  still  be  easily 


DISORDERS    OF    SLEEP  455 

wakened  by  moderate  stimuli  such  as  ordinary  conversation,  light 
touches,  &c.  A  deeper  stage  is  sleep  with  dreams,  where  the 
sleeper  is  unconscious  of  his  surroundings  but  yet  hLs  psychical 
centres,  uncontrolled  and  deprived  of  the  faculty  of  comparison 
with  his  environment,  produce  a  series  of  fantastic  mental  pictures. 
Under  the  influence  of  dreams  a  sleeper  may,  if  his  cortical  motor 
centres  are  still  active  whilst  the  psycho -sensory  centres  are  un- 
controlled, perform  motor  actions,  as  in  the  well-known  stage  of 
sleep  with  somnambulism.  But  somnambulism  is  rare  in  health, 
because  ordinarily  the  cortical  motor  centres  are  dulled  simul- 
taneously with  the  sensory.  Still  more  profound  is  the  stage  of 
deep  dreamless  sleep.  This  variety  merges  into  what  under  patho- 
logical conditions  we  call  stupor  and  ultimately  coma.  The  chief 
distinguishing  point  between  deep  sleep  and  coma  is  that  a  sleeping 
person  can  be  roused  whereas  a  comatose  patient  cannot. 

Disorders  of  Sleep. — We  sometimes  meet  with  pathological 
drowsiness  or  hypersomnia,  which  is  most  frequently  associated 
with  some  variety  of  toxaemia.  Perhaps  the  most  common 
instance  is  that  of  an  anaemic  young  woman.  Here  the 
droAvsiness  may  be  partly  toxic,  due  to  absorption  of  poisons, 
whether  from  a  loaded  intestine,  from  decaying  teeth,  or 
from  other  sources,  but  the  main  element  in  causation  is 
probably  vascular.  In  such  a  case  the  heart  is  devoid  of 
energy,  and  the  vessels  throughout  the  body  are  flabby  and 
deficient  in  tone.  Therefore  in  the  erect  attitude  the  vessels  of  the 
brain  are  badly  filled,  and  if  the  patient  sits  down  during  the  day 
she  feels  drowsy.  But  when  she  lies  down  at  night,  the  brain  now 
becomes  hypersemic  from  want  of  vascular  tone,  and  the  result  is 
that  she  lies  awake.  This  combination  of  diurnal  drowsiness  with 
nocturnal  wakefulness  is  highly  characteristic.  In  treating  the 
condition,  besides  attacking  the  anaemia,  we  often  administer 
digitalis,  since,  besides  being  a  cardiac  tonic,  it  has  also  a  well- 
marked  vaso -constrictor  action.  If  digitahs  be  combined  with 
iron  and  with  bromide  of  potassium,  the  condition  usually 
improves  rapidly. 

Drowsiness  also  occurs  in  other  conditions.  Myxedematous 
patients  are  habitually  sleepy  and  stupid,  probably  from  toxsemia 
and  thyroid  insufficiency.  So  also  are  many  idiots  and 
cretins.  After  a  severe  fit  of  epilepsy  it  is  common  for  the 
patient    to   fall    into    a    deep    'post-epileptic   sleep,    largely    due, 


456  NERVOUS    DISEASES 

no  doubt,  to  toxic  products  produced  by  the  nervous  and 
muscular  systems  during  the  fit.  Certain  tumours  of  the  brain, 
especially  those  in  the  region  of  the  floor  of  the  third  ventricle, 
as  we  have  already  seen,  are  associated  with  early  and  persistent 
drowsiness  ;  so  also  are  some  cases  of  punctured  wounds  in  the 
same  region.^  Elsewhere  in  the  brain,  tumours  may  also  produce 
drowsiness  at  a  late  stage  of  the  disease,  probably  from  increased 
intra -cranial  pressure,  though  in  these  cases  the  condition  more 
nearly  approaches  coma  and  ultimately  merges  into  it.  The 
intense  drowsiness  produced  by  the  combination  of  exhaustion 
with  extreme  cold,  as  in  arctic  travellers  or  alpine  climbers 
who  are  in  danger  of  being  frozen  to  death,  is  probably 
largely  due  to  deficient  circulation,  and  unless  vigorous  meas- 
ures be  taken  to  stimulate  the  heart  and  the  general  circula- 
tion, sleep  passes  on  to  coma  and  death.  The  hibernation-sleep 
of  certain  animals  is  largely  due  to  winter-cold,  for  if  such 
animals  be  kept  in  a  warm  atmosphere  throughout  the  winter, 
they  do  not  sleep  more  than  in  summer  time.  The  delightful 
drowsiness  produced  by  gazing  into  a  red  fire  on  a  winter  afternoon 
is  something  entirely  different.  It  is  probably  a  mild  variety  of 
hypnotic  sleep,  the  continuous  red  glow  acting  through  the  optic 
nerves  by  a  summation  of  stimuli.  It  is  not  a  question  of  the 
mere  heat  of  the  fire,  for  unless  the  blaze  be  seen,  drowsiness  is 
less  likely  to  supervene.  A  similar  summation  of  stimuli  probably 
explains  the  well-known  church  drowsiness.  The  soothing  mono- 
tony of  the  sermon,  combined  with  the  sitting  posture  of  the 
listener  (who  thus  has  the  additional  excuse  of  a  degree  of  cerebral 
ansemia),  and  lastly  the  common  habit  of  closing  the  eyes  to  avoid 
visual  distractions,  all  these  combine  to  make  church-drowsiness 
a  popular  disorder.  I  do  not  refer,  of  course,  to  wild  "  revival " 
meetings,  nor  to  militant  political  or  sensational  sermons,  where 
the  conditions  both  of  preacher  and  of  audience  are  entirely 
different. 

But  there  are  other  pathological  varieties  of  sleep  to  which  we 
must  refer.  There  is  the  drowsiness  of  impending  urcemic  or 
diahetic  coma,  both  toxic  in  origin.  There  is  also  that  remarkable 
tropical  disease,  sleeping-sickness,  endemic  in  certain  parts  of 
Africa,  and  associated  with  the  presence  of  trypanosomes  in  the 
blood,  glands,  and  cerebro-spinal  fluid.  The  drowsiness  in  this 
1  Knagg,  Lancet,  1907,  p.  1477. 


DISORDERS    OF    SLEEP  457 

malady  is  doubtless  due  to  some  toxin  produced  by  the  parasites. 
In  the  later  stages  of  the  disease  a  peri-vascular  cellular  inJEiltra- 
tion  is  found  around  the  cerebral  vessels,  a  variety  of  chronic 
meningo-encephalitis.  Ankylostomiasis  often  produces  drowsiness, 
probably  from  toxic  absorption  resulting  from  the  intestinal 
parasites.  Narcolepsy  is  another  condition  in  which  the  patient 
has  sudden  paroxysms  of  sleep,  in  the  midst  of  whatever  occu- 
pation he  may  be  pursuing  at  the  moment.  These  cases  are 
hysterical.  I  remember  one  such  patient  who  used  to  fall  asleep 
when  playing  the  piano  or  during  a  game  of  cards  (especially  if  he 
held  a  losing  hand).  He  had  numerous  other  hysterical  stigmata, 
and  the  diagnosis  presented  no  serious  difficulty.  The  hypiwHc 
trance  is  another  condition,  analogous  in  some  respects  to  ordinary 
sleep,  but  time  does  not  allow  us  to  discuss  it  here.  Suffice  it  to 
say  that  the  phenomena  of  hypnosis  can  be  induced  by  repeated 
monotonous  stimuli,  visual,  auditory  or  otherwise,  aided  by  sugges- 
tion. The  patient  is  thereby  made  to  fall  into  a  sleepy  condition, 
varying  in  intensity  from  mere  drowsiness  to  dreams  (the 
incidents  of  which  are  controlled  by  suggestion),  to  somnam- 
bulism, or  to  deep  dreamless  slumber  lasting  perhaps  for  many 
hours.  There  are  also  the  well-known  phenomena  of  spon- 
taneous somnambulism,  due  to  the  remaining  awake,  as  it  were, 
of  the  cortical  motor  centres  when  the  higher  sensory  and 
psychical  centres  have  lost  their  power  of  inhibition.  Such  a 
patient  gets  up  and  acts  his  dream.  Nightmares  are  horrifying 
dreams  associated  with  a  feeUng  of  agonising  helplessness,  and 
producing  so  much  distress  that  they  sometimes  waken  the  patient 
up  in  a  state  of  dyspnoea.  They  are  generally  toxic  in  origin. 
Their  commonest  cause  is  gastro -intestinal  fermentation,  certain 
articles  of  diet  (proverbially  a  lobster  supper)  being  specially  Hable 
to  produce  bad  dreams.  In  children  nightmares  often  recur  again 
and  again  with  the  peculiarity  that  the  terrifying  hallucination 
is  the  same  on  each  occasion.  Here  again  gastro-intestinal  fer- 
mentation is  often  a  factor.  Still  more  frequently  do  we  find  that 
the  child  has  adenoids,  which  interfere  with  respiration  and  produce 
a  degree  of  carbon  dioxide  poisoning.  Removal  of  adenoids  and 
attention  to  the  bowels  cure  most  cases  of  night-terrors  in  children. 
Patients  with  tropical  abscess  of  the  liver,  curiously  enough,  are 
particularly  liable  to  horrible  dreams,  so  much  so  that  they  may  be 
afraid  to  fall  asleep.     Here  again  the  condition  is  doubtless  toxic. 


458  NERVOUS    DISEASES 

Nightmare  is  also  a  frequent  symptom  in  patients  witli  aortic 
regurgitation.  In  them  the  condition  is  not  toxic  but  vascular  in 
origin,  due  to  irregularity  in  the  blood-supply  and  to  pulsation  in 
the  cortical  capillaries. 

Lastly  let  us  consider  the  subject  of  sleeplessness  or  insomnia. 
Cases  of  insomnia  may  be  divided  into  two  great  classes,  the 
extrinsic  and  the  intrinsic. 

Extrinsic  insomnia  includes  those  cases  in  which  the  sleeplessness 
is  secondary  to  some  outside  cause,  not  directly  arising  in  the 
cerebrum  or  its  blood-vessels.  For  example,  physical  pain  of  any 
sort,  cough,  vomiting,  frequent  micturition,  diarrhoea,  pruritus, 
and  so  on,  may  keep  a  patient  awake.  In  all  such  cases  we  must 
treat  the  primary  symptom ;  when  it  is  relieved,  sleep  will  follow 
naturally.  This  group  also  includes  emotional  insomnia,  which 
is  more  often  the  result  of  grief  than  of  joy,  and  more  commonly 
associated  with  fear  or  apprehension  for  the  future,  than  with 
remorse  or  sorrow  for  the  past.  When  pleasurable  emotion  does 
cause  insomnia,  it  is  generally  due  to  anticipation  of  some  happiness 
in  the  immediate  future.  A  man  does  not  usually  lie  awake  because 
some  one  is  going  to  leave  him  a  fortune  twenty  years  hence,  but 
he  may  spend  a  sleepless  night  on  the  eve  of  his  wedding.  The 
treatment  of  emotional  insomnia,  apart  from  assuaging  the  patient's 
sorrow  (a  matter  which  is  often  beyond  the  physician's  sphere), 
is  best  accomplished  by  giving  some  cerebral  sedative,  such  as 
a  mixture  of  chloral  and  potassium  bromide.  The  insomnia  of 
extreme  joy  seldom  calls  for  treatment,  but  if  the  patient  becomes 
too  excited,  here  again  a  cerebral  sedative  may  be  given. 

We  are  much  oftener  consulted  with  regard  to  the  other  kind 
of  insomnia,  which  we  may  call  intrinsic  insomnia.  This  is 
commonly  due  to  vascular,  toxic,  or  nervous  faults,  or  to  com- 
binations of  all  three. 

As  to  vascular  causes,  the  brain  may  be  hypersemic,  rendering 
sleep  impossible.  Hyperaemic  insomnia  may  be  either  of  the  high- 
tension  or  of  the  low-tension  type.  In  high-tension  insomnia  the 
patient  may  be  the  subject  o'^  general  arterio -sclerosis  or  of  renal 
disease,  and  the  hyper-tension  is  readily  demonstrated  by  the 
Riva-Rocci  sphygmo- manometer.  In  such  cases  the  patient 
complains  of  a  difficulty  in  falling  off  to  sleep.  A  useful  remedy 
for  this  is  to  relax  the  vessels  by  some  vaso-dilator  such  as  erythrol 
tetranitrate,  and  to  give  a  mercurial  aperient  such  as  blue  pill 


DISORDERS    OF    SLEEP  459 

or  calomel,  say  two  or  three  times  a  week.  This  often  brings 
down  the  tension  in  a  remarkable  way  and  induces  sleep.  Of 
course  we  also  lay  down  careful  regulations  as  to  diet,  &c., 
in  these  cases.  Hypersemic  insomnia  from  low  tension  occurs  in 
anaemic  and  neurasthenic  patients,  as  already  explained,  and  is 
characterised  by  the  fact  that  when  the  patient  sits  erect  in  a 
chair  he  becomes  drowsy,  whereas  when  he  lies  down  in  bed 
the  brain  becomes  over-filled  with  blood  and  the  patient  cannot 
get  to  sleep.  In  such  cases  the  best  remedy  is  a  combination  of 
a  cardio-vascular  tonic  like  digitalis  with  a  moderate  dose  of 
bromide  of  potassium.  Hypersemic  insomnia,  whether  of  high- 
tension  or  of  low-tension  type,  is  often  associated  with  cold  feet. 
If  the  feet  can  be  made  warm,  the  cerebral  hypereemia  tends  to 
become  alleviated.  A  cup  of  hot  milk  or  hot  soup,  by  producing 
abdominal  hypersemia,  often  relieves  hypersemic  insomnia. 

Insomnia  is  one  of  the  most  distressing  symptoms  of  chronic 
heart-failure.  Just  when  dropping  oS  to  sleep  the  patient  suddenly 
starts  awake  with  a  feeling  of  suffocation,  gasping  for  breath. 
This  is  probably  due  to  deficient  circulation  in  the  medulla 
oblongata.  We  treat  the  condition  by  cardiac  tonics,  together 
with  one  of  the  non-depressant  pure  hypnotics,  or  even  by  morphia, 
cautiously  administered  and  combined  with  atropine. 

Next  we  have  toxic  insomnia,  which  is  one  of  the  commonest 
varieties  met  with  in  practice.  Many  cases  are  associated  with 
gastric  or  intestinal  fermentation,  and  especially  with  dilatation 
of  the  stomach.  The  symptoms  are  characteristic.  The  patient 
falls  asleep,  but,  after  an  hour  or  two,  varying  according  to  the 
degree  of  gastric  dilatation,  he  wakes  up,  perhaps  after  a  horrible 
dream,  with  palpitation,  profuse  sweating  or  gastric  uneasiness. 
He  may  have  a  sinking  feeling  with  craving  for  food,  and  if  he 
eats  a  biscuit  or  some  other  simple  food,  the  stomach  contents 
are  temporarily  diluted  and  he  feels  reHeved  for  the  time.  This 
may  mislead  him  into  thinking  that  his  sleeplessness  is  due  to 
exhaustion  from  want  of  food,  which  is  far  from  the  fact.  During 
his  waking  hours  he  is  often  very  depressed,  hypochondriac,  and 
almost  melancholic.  When  we  have  a  clinical  history  of  this 
sort,  we  should  carefully  examine  the  abdomen.  If  we  find  the 
physical  signs  of  dilated  stomach,  we  treat  the  patient  accordingly, 
putting  him  on  a  dry  dietary,  free  from  starchy  foods  or  green 
vegetables,  and  attending  carefully  to  the  bowels.     Meanwhile  we 


460  NERVOUS    DISEASES 

administer  gastro-intestinal  antiseptics  such  as  carbolic  acid, 
creasote,  /3  naphthol,  or  sulpho-carbolate  of  soda.  To  give  hypnotics 
in  such  cases,  without  correcting  the  gastric  condition,  is  worse 
than  useless. 

Amongst  the  toxic  forms  of  insomnia  we  must  not  omit  to 
refer  to  the  sleeplessness  produced  by  chronic  excess  in  alcohol, 
culminating  sometimes  in  delirium  tremens,  also  the  insomnia  of 
acute  fevers.  Both  in  fever  and  in  delirium  tremens,  sleep  can 
often  be  induced  by  a  cold  pack  or  cold  sponging.  Insomnia  may 
result  sometimes  from  excessive  tobacco  smoking,  which  produces 
its  effect  partly  by  its  action  on  the  nerve-cells,  partly  by  its 
influence  on  the  circulation.  Strong  tea  or  coffee  may  also  act 
in  a  similar  fashion,  keeping  a  patient  awake.  Insomnia  may 
occur  in  secondary  or  tertiary  syphilis,  even  apart  from  the 
familiar  nocturnal  headache :  this  variety  yields  promptly  to 
mercury. 

'  Lastly,  there  is  primary  or  "  nervous  "  insomnia,  due  to  over- 
fatigue, especially  from  mental  over-work.  We  see  many  instances 
amongst  busy  professional  or  business  men.  But  in  most  cases 
there  are  several  factors  involved,  not  only  the  toxins  of  exhaustion 
but  those  of  hasty  and  ill-digested  meals,  together  with  a  suc- 
cession of  powerful  mental  stimuli,  and  the  persistent  cerebral 
hypergemia  of  the  brain-worker. 

In  every  case  of  primary  insomnia,  besides  correcting  any  gastric, 
intestinal,  or  vascular  fault  that  may  be  present,  we  should  make 
it  a  golden  rule  to  send  the  patient  away  for  a  complete  holiday. 
These  are  also  the  cases  for  the  employment  of  the  pure  hypnotics, 
which  have  a  direct  sedative  action  on  the  psycho -sensory  cortex. 
The  name  of  these  drugs  is  legion,  and  I  do  not  propose  to  discuss 
them  exhaustively.  Amongst  the  most  reliable  is  paraldehyde. 
Its  somewhat  nauseous  taste  is  no  drawback,  since  it  prevents 
the  patient  from  acquiring  a  habit  for  the  drug.  Of  the  other 
hypnotics  I  need  only  mention  a  few,  such  as  chloral  hydrate, 
sulphonal,  and  veronal.  We  should  never  allow  a  patient  carte 
blanche  to  take  a  hypnotic  drug  on  his  own  initiative.  Self- 
drugging  with  hypnotics  is  highly  dangerous.  No  hypnotic  should 
ever  be  taken  without  the  express  authority  of  the  physician. 
Nor  should  any  one,  even  though  he  be  a  medical  man,  prescribe 
hypnotics  for  himself ;  he  should  call  in  a  professional  colleague. 

Drugs  like  hyoscine  and  morphia  are  our  last  resort  in  obstinate 


DISORDERS    OF    SLEEP  461 

insomnia.  In  severe  cases  of  excited  mania  or  melancholia  gr.  y^^ 
of  hyoscine,  hypodermically,  or  gr.  ^-  of  morphine  with  gr.  1^77  of 
atropine,  soothe  the  patient  in  a  remarkable  way.  Persistent 
insomnia  in  cases  of  insanity  is  of  serious  omen.  Most  alienist 
physicians  insist  on  having  charts  kept  of  the  amount  of  sleep 
obtained  by  each  insane  patient,  since  severe  insomnia  recurring 
regularly  for  a  month  in  cases  of  insanity  renders  the  prognosis 
as  to  recovery  very  unfavourable. 


CHAPTER  XXy 

INTEA-CEANIAL   TUMOURS 

For  clinical  purposes  we  include  under  tMs  heading  not  only  the 
neoplasms  proper  (glioma,  sarcoma,  endothelioma,  fibroma,  carci- 
noma, &c.),  but  also  gummatous  and  tuberculous  growths,  para- 
sitic and  other  cysts,  aneurisms,  and  even  abscesses.  All  of  these 
may  be  regarded  as  slowly-growing  foreign  bodies  which,  sooner 
or  later,  according  to  their  situation  within  the  cranial  cavity, 
produce  clinical  phenomena  which  render  their  diagnosis  possible. 
Progressive  cerebral  lesions,  as  a  rule,  produce  their  effects  not  so 
much  by  destruction  of  brain  substance,  but  mainly  by  interference 
with  the  circulation  in  the  affected  region  of  the  brain,  together  with 
displacement,  distortion,  and  compression  of  the  nerve  elements. 
Only  in  a  few  instances  {e.g.  in  carcinoma,  melanotic  sarcoma) 
are  the  nerve  elements  directly  destroyed  by  the  tumour  cells. 
The  importance  of  the  circulatory  element  is  shown  by  the  fact 
that  paralytic  focal  symptoms  may  completely  clear  up  after  the 
evacuation  of  an  abscess  or  hsematoma,  or  after  a  decompressive 
operation  for  tumour.  Moderate  compression  produces  local 
venous  engorgement  with  increased  excitabihty  of  the  brain-tissue  ; 
further  increase  of  the  abnormal  pressure  produces  local  cerebral 
anaemia,  with  loss  of  function  and  paralytic  phenomena. 

Two  classes  of  signs  and  symptoms  occur  :  firstly,  general  symp- 
toms of  increased  intra-cranial  pressure,  independent  of  the  posi- 
tion of  the  tumour,  and  secondly,  focal  symptoms,  which  vary 
according  to  the  particular  part  of  the  brain  implicated  by  the 
growth.  General  symptoms  enable  us  to  say  that  there  is  a 
tumour  somewhere  within  the  skull ;  in  order  to  locate  the 
growth  precisely,  we  must  search  for  locahsing  symptoms  which 
are  usually,  though  not  necessarily,  later  in  onset.  If  localising 
symptoms  are  absent,  focal  diagnosis  may  be  impossible. 
l^fGeneral  Symptoms.  —  The  cardinal  phenomena  of  intra- 
cranial tumour  are  three  in  nimaber,  viz.  headache,  optic  neuritis, 

462 


INTRA-CRANIAL    TUMOURS  463 

and  vomiting.  To  these  may  be  added  others,  such  as  mental 
changes,  generalised  convulsions,  giddiness,  slowing  of  the  pulse,  &c. 
The  triad  syndrome  of  headache,  optic  neuritis,  and  vomiting  should 
always  suggest  the  possible  presence  of  an  intra-cranial  growth. 
But  before  diagnosing  cerebral  tumour  from  these  three  signs 
alone,  we  must  be  careful  to  exclude  three  other  conditions,  any 
of  which  may  produce  the  triad  syndrome.  These  conditions  are 
kidney  disease,  severe  anaemia,  and  lead-poisoning,  all  of  them 
easy  of  recognition  if  we  bear  the  point  in  mind. 

Headache  is  the  most  constant  symptom  of  intra-cranial  tumour  ; 
it  generally  appears  at  some  period  or  other,  sooner  or  later.  Its 
severity  is  sometimes  intense.  Usually  it  is  a  constant  dull  pain 
with  paroxysms  of  agonising  intensity.  The  pain  may  be  diffuse 
or  localised.  If  localised,  its  position  does  not  necessarily  corre- 
spond with  the  situation  of  the  tumour,  except  with  tumours  at  or 
near  the  surface  of  the  brain,  when  the  pain  may  sometimes  be 
directly  over  the  growth  and  accompanied  by  local  tenderness 
on  percussion  or  pressure,  or  even  by  a  local  alteration  of  percussion- 
note.  But  too  much  stress  should  not  be  laid  on  the  existence 
of  localised  pain,  unless  accompanied  by  other  focal  signs.  Thus, 
for  example,  cerebellar  tumours  often  produce  frontal  headache, 
and  in  one  case  of  my  own  ^  a  right-sided  cerebellar  growth  was 
accompanied  by  pain  hmited  to  the  left  frontal  region.  The 
headache  of  intra-cranial  tumour  is  intensified  by  excitement,  by 
exertion,  or  by  any  temporary  cerebral  hypersemia. 

Opic  neuritis  or  "  choked  disc,"  detected  with  the  ophthalmo- 
scope, should  be  looked  for  in  every  case  of  suspected  intra-cranial 
tumour.  But  it  should  be  borne  in  mind  that  while  the  presence 
of  optic  neuritis  is  one  of  the  strongest  evidences  of  intra-cranial 
mischief,  no  weight  should  be  laid  on  its  absence  if  other  signs 
point  to  intra-cranial  growth.  Even  apart  from  actual  neuritis, 
increased  intra-cranial  pressure  often  causes  a  concentric  limi- 
tation of  the  visual  field  for  blue.  This  may  even  amount  to  blue- 
blindness.2  Optic  neuritis  from  brain  tumour  is  relatively  more 
frequent  in  hypermetropic  than  in  myopic  eyes.^  Another  point 
of  importance  is  that  intense  optic  neuritis  may  coexist  with 
perfect  vision.     But  in  time,  optic  neuritis  generally  progresses  to 

^  Edin.  Hosp.  Reports,  1895.    An  almost  identical  case  has  been  recorded 
by  Sachs  (Medical  Record,  December  22,  1906). 

^  Gushing,  Johns  Hopkins  Hosp.  Bulletins,  1909,  xx.  p.  95. 
3  Gunn,  Brit.  Med.  Journ.,  1907,  p.  1126. 


464  NEEVOUS    DISEASES 

optic  atrophy,  with  its  accompanying  blindness.  Many  patients 
with  intra-cranial  tumour  have  early  transient  blindness,  some- 
times momentary,  sometimes  lasting  for  a  few  hours  or  days  at  a 
time,  in  one  or  both  eyes.  Trephining  the  skull  and  opening  of 
the  dura  mater  generally  reheve  optic  neuritis  even  though  the 
growth  be  not  removed ;  they  also  give  considerable  rehef  to 
the  headache.  The  optic  neuritis  of  brain  tumours,  though  gener- 
ally affecting  both  eyes,  may  be  unequal  on  the  two  sides,  or  it 
may  even  be  uniocular.  On  the  whole,  the  greater  intensity  tends 
to  be  on  the  same  side  as  the  tumour,  especially  in  frontal  and 
cerebellar  tumours,  though  this  rule  is  not  invariable.  In  cere- 
bellar tumours  optic  neuritis  is  specially  early  in  onset. 

Vomiting  is  a  less  constant  phenomenon  than  headache  and 
optic  neuritis,  except  in  tumours  of  the  posterior  fossa,  in  which, 
from  the  very  outset,  it  is  rarely  absent.  "  Cerebral "  vomiting 
differs  from  the  ordinary  vomiting  of  abdominal  disorders.  It 
usually  occurs  independently  of  food,  and  is  unassociated  with 
other  gastro -intestinal  symptoms.  Moreover,  it  is  often  unpreceded 
by  nausea  and  thus  has  a  curious  "  projectile "  character.  A 
change  of  posture  of  the  head  is  sometimes  enough  to  induce  an 
attack  of  cerebral  vomiting. 

Amongst  the  other  '  general '  symptoms  we  must  mention 
'progressive  mental  dulness.  This  is  apparently  to  a  large  extent 
the  result  of  increased  intra-cranial  pressure  and  of  persistent 
headache.  The  patient  becomes  apathetic,  dull,  and  slow  in 
answering  questions ;  he  loses  interest  in  his  ordinary  affairs. 
Sometimes  he  becomes  overwhelmingly  drowsy  and  finally  comatose. 
In  the  later  stages  the  sphincters  are  uncontrolled.  Mental  changes 
are  particularly  early  of  onset  in  tumours  of  the  pre-frontal  region, 
altogether  independently  of  the  intensity  of  the  headache. 

Generalised  epileptiform  convulsions  (as  distinguished  from 
Jacksonian  attacks)  may  be  produced  by  tumours  in  almost  any 
part  of  the  brain,  not  necessarily  in  the  immediate  neighbourhood 
of  the  motor  areas.  Such  convulsions  probably  result  mainly 
from  increased  intra-cranial  pressure  and,  as  a  rule,  occur  com- 
paratively late  in  the  disease.  But  they  may  also,  though  less 
commonly,  appear  as  the  initial  symptom  of  an  intra-cranial 
growth.  In  such  cases  epilepsy  is  sometimes  diagnosed,  and 
until  further  phenomena  (such  as  optic  neuritis  or  focal  signs) 
develop,   the   error  is   unavoidable.       More  usually  general  con- 


INTRA-CRANIAL    TUMOURS  465 

vulsions  are  a  late  phenomenon,  and  there  are  antecedent  physical 
signs  to  guide  us. 

Attacks  of  giddiness  are  often  complained  of  in  brain  tumour. 
Sometimes  these  are  merely  indescribable  feelings  of  confusion  ; 
in  other  cases  there  is  a  true  vertigo  or  feeling  of  uncertainty  in 
equilibration.  Vertigo  is  specially  early  and  severe  with  tumours  of 
the  cerebellum,  cerebellar  peduncles,  and  corpora  quadrigemina, 
and  in  such  cases  is  often  associated  with  the  motor  phenomenon  of 
a  reeling  or  staggering  gait. 

Slowing  of  the  fulse,  permanent  or  transient,  is  a  valuable 
corroborative  sign  of  intra -cranial  abscess.  It  may  also  occur  as 
one  of  the  general  symptoms  of  tumour,  especially  in  the  neigh- 
bourhood of  the  medulla  oblongata.  In  other  cases,  again,  we 
may  meet  with  tachycardia.  Therefore  the  pulse-rate  of  itself 
is  not  of  high  diagnostic  significance,  compared  with  the  other 
signs  already  mentioned.  Slowness  of  breathing  and  a  Cheyne- 
Stokes  type  of  respiration  may  occur,  but  mostly  in  the  latest 
stages  of  the  disease.  Paroxysms  of  yawning  or  of  hiccough  may 
also  be  produced  by  intra -cranial  growths,  especially  those  of  the 
posterior  fossa. 

Localising  symptoms  are  sometimes  absent,  and  a  tumour 
may  only  be  revealed  by  post-mortem  examination.  This 
experience  is  commoner  with  temporal  tumours  than  with  those 
occurring  elsewhere.  In  most  cases,  however,  focal  symptoms 
develop,  which  enable  us  to  determine  the  position  of  the  growth 
with  greater  or  less  precision.  In  a  few  cases  radiography  may 
reveal  an  abnormal  shadow  in  the  position  of  the  tumour.  With 
superficial  tumours  local  percussion  of  the  skull  may  occasionally 
yield  an  altered  note.  But  in  some  cases  we  can  only  form  an 
approximate  idea  as  to  the  site  of  the  disease.  For  example,  if  a 
patient  with  headache,  vomiting,  and  optic  neuritis  develops  a 
gradually  increasing  left  hemiplegia,  all  that  we  are  justified  in 
diagnosing  is  a  growth  somewhere  in  the  right  cerebral  hemi- 
sphere, probably  in  the  neighbourhood  of  the  motor  tract.  Unless 
additional  signs  appear,  it  may  be  impossible  to  say  more,  since 
such  hemiplegia  may  be  produced  not  only  by  tumours  directly 
implicating  the  pyramidal  tract,  but  also  by  frontal,  temporal,  or 
even  occipital  tumours  compressing  the  motor  path.  Again,  the 
occurrence  of  cranial  nerve  palsies  is  always  suggestive  of  a  lesion 
at  the  base  of  the  brain  ;    but  this  rule  is  not  invariable.     For 

2  G 


466 


NERVOUS   DISEASES 


example,  isolated  ocular  palsy  of  one  external  rectus  has  little  or 
no  localising  value,  since  the  sixth  nerve  may  be  paralysed  (whether 
from  traction  or  from  increased  intra-cranial  pressure)  by  a  growth 
anywhere  within  the  skull.  Further,  we  may  have  "  false  localising 
signs  "  ^  from  compression  or  distortion  by  growths  in  distant 
parts  of  the  brain.  Thus,  for  example,  a  tumour  of  the  frontal 
lobe  may  at  a  later  stage  produce  signs  of  contra -lateral  cerebellar 
disease,  or  a  cerebellar  growth  may  afterwards  be  associated  with 


Fig.  226. — Tumour  of  right  cerebral  hemisphere  in  a  man  of  47.  The  clinical 
signs  were  headache,  vomiting,  double  optic  neuritis,  progressive  mental 
dulness  and  ultimately  slight  paresis  of  the  left  face,  arm  and  leg,  with 
absence  of  the  left  knee- and  ankle-jerk  and  an  inconstant  left-sided  extensor 
plantar  response. 


Jacksonian  fits  of  one  limb,  suggestive  of  a  lesion  of  the  motor 
area,  but  really  due  to  distension  of  the  lateral  ventricle  of  the 
corresponding  side,  and  so  on.  Or  again,  localising  symptoms  may 
be  masked  or  concealed,  as  in  some  cases  of  occipital  tumour  in  which, 
if  the  optic  neuritis  goes  on  to  atrophy  and  blindness,  the  hemi- 
anopia,  which  might  have  led  to  a  correct  diagnosis,  becomes  lost. 
Localising  signs,  to  be  of  value,  should  generally  appear  early.  Ab- 
sence of  local  signs  suggests  that  the  tumour  is  above  the  tentorium, 
seeing  that  sub-tentorial  growths  almost  always  produce  localising 
signs  early  in  their  course. 

1  Collier,  Brain,  1904,  p.  490. 


INTRA-CRANIAL    TUMOURS 


467 


Bearing  the  above  points  in  mind,  let  us  now  consider  the  chief 
localising  symptoms  of  tumours  in  the  various  regions  of  the  brain. 

Tumours  of  the  Motor  Cortex. — The  motor  area,  as  we  have 
already  seen,  comprises  the  pre-central  convolution  and  the  ad- 
jacent end  of  the  second  frontal  gyrus,  together  with  part  of  the 
cortex  on  the  mesial  surface  of  the  hemisphere.  Tumours  of  the 
motor  region  are  the  easiest  of  all  to  recognise  clinically.     In  them, 


Fig.  227. — Endothelioma  of  meninges  invading  right  pre-central  gyrus  in  its 
upper  third.  The  positions  of  the  fissures  of  Rolando  are  indicated  by  a 
series  of  black  beads.  The  patient  had  Jacksouian  convulsions  commencing 
with  a  painful  spasm  of  the  left  foot.  There  was  paresis  of  the  left  leg  and, 
to  a  less  extent,  of  the  left  arm.  The  face  was  unaffected.  There  was  no 
sensory  impairment. 

in  addition  to  the  general  signs  of  intra-cranial  tumour,  we  usually 
observe  two  classes  of  phenomena,  irritative  and  paralytic. 

The  irritative  group  consists  of  Jacksonian  fits,  commencing  in 
the  contra-lateral  face,  tongue,  arm,  or  leg,  as  the  case  may  be, 
according  to  the  part  of  the  motor  cortex  which  happens  to  be 
chiefly  implicated.  In  a  Jacksonian  fit  the  convulsion,  which 
usually  consists  of  tonic  spasm  followed  by  clonic  jerks,  may  be 
strictly  localised  to  a  small  group  of  muscles,  or  it  may  spread  from 
them  to  other  muscle-groups,  but  always  in  a  regular  order  (as 
shown  in  Fig.  3,  p.  5).     Less  commonly  the  whole  of  the  muscles 


468  NERVOUS   DISEASES 

of  the  contra-lateral  face,  arm,  and  leg  are  thrown  into  convulsion 
simultaneously.  Jacksonian  convulsions  differ  from  ordinary  epi- 
lepsy in  that  the  patient  usually  retains  consciousness  all  the  time, 
and  can  study  his  own  fit.  But  if  the  convulsion  spreads  across 
the  middle  line  and  becomes  bilateral,  consciousness  becomes  lost 
at  or  before  the  moment  of  crossing. 

The  paralytic  phenomena,  in  tumours  of  the  motor  region,  consist 
in  weakness  of  the  convulsed  muscles  during  the  inter-paroxysmal 
periods  (see  Figs.  37  and  38,  p.  81).  Such  weakness  is  most 
marked  immediately  after  a  convulsion.  There  is  also  temporary 
atopognosis  in  the  affected  limb  and  loss  of  the  sense  of  position. 

According  as  the  growth  is  primarily  cortical  or  sub-cortical, 
convulsions  precede  muscular  weakness  or  vice  versd.  A  cortical 
tumour,  for  example  one  growing  from  the  meninges,  is  irritative 
from  the  first ;  a  sub-cortical  growth  is  usually  indicated  by  an 
initial  monoplegia,  followed  later  by  Jacksonian  convulsions. 
Moreover,  in  a  sub-cortical  growth  the  precise  starting-point  of 
the  convulsions  is  less  constantly  localised  to  the  same  muscle - 
group  ;  thus,  for  example,  a  sub-cortical  tumour  immediately 
under  the  arm-area  may  produce  Jacksonian  fits,  commencing 
sometimes  in  the  thumb,  at  other  times  in  the  elbow.  The  extent 
of  a  Jacksonian  fit  also  varies  with  the  extent  of  the  tumour.  A 
small  superficial  tumour  will  produce  a  highly  localised  fit  followed 
by  monoplegia  of  the  affected  part,  whereas  a  tumour  of  the  same 
size,  situated  deeper  beneath  the  cortex,  will  produce  an  initial 
monoplegia,  convulsions  being  weeks  or  months  later  in  onset. 
The  deeper  the  growth,  the  less  tendency  is  there  to  localised  con- 
vulsions. Tumours  of  the  pre-central  or  motor  area,  if  extending 
backwards  across  the  Rolandic  fissure  to  the  post-central  convolu- 
tion, are  usually  associated  with  a  distinct  sensory  aura  in  the 
affected  limb  at  the  beginning  of  the  motor  convulsion,  together 
with  a  degree  of  anaesthesia,  monoplegic  or  hemiplegic  in  distribu- 
tion. The  differences  between  cortical  and  sub-cortical  types  of 
anaesthesia  have  already  been  discussed  (p.  208). 

Tumours  of  the  Frontal  Region. — For  clinical  purposes  this 
region  of  the  brain-cortex,  anterior  to  the  motor  area  proper,  may 
be  subdivided  into  two  parts  :  (1)  A  pre-frontal  or  higher  psychical 
area,  devoid  of  motor  centres.  This  area,  when  electrically 
stimulated,  produces  no  convulsion.  (2)  A  post-frontal  area,  con- 
tinuous posteriorly  with  the  pre-central  convolution  and  including 


INTRACRANIAL    TUMOURS  469 

the  cortical  centre  for  conjugate  deviation  of  the  head  and  eyes 
towards  the  opposite  side.  On  the  left  side  it  contains,  in  addi- 
tion, the  cortical  motor  centres  for  spoken  words. 

Pre-frontal  tumours,  besides  producing  the  general  signs  of 
cerebral  tumour,  tend  to  excite  mental  symptoms  specially  early, 
consisting  in  dulness,  failure  of  memory,  tendency  to  childish 
jocularity,  deficiency  of  attention,  and  neglect  of  the  sphincters. 
These  mental  symptoms  are  equally  likely  to  occur  with  tumours 
of  the  right  side  and  of  the  left.^  Some  pre-frontal  tumours,  how- 
ever, produce  no  mental  symptoms  at  all.  Post-frontal  tumours 
cause,  in  addition,  local  Jacksonian  fits,  especially  attacks  beginning 
with,  or  consisting  entirely  in,  deviation  of  the  head  and  eyes  to  the 
contra-lateral  side.  Bianchi  '  has  described  paroxysmal  dilatation 
and  contraction  of  the  contra-lateral  pupil — pupillary  Jacksonian  fits 
— in  cases  of  pre-frontal  tumour.  With  left-sided  tumours  we  may 
have  fits  commencing  with  sudden  attacks  of  motor  aphasia  (though 
the  absence  of  aphasia  does  not  necessarily  exclude  a  diagnosis  of  left- 
sided  post-frontal  growth).  General  epileptiform  convulsions,  and 
even  attacks  of  petit  mal,  are  not  uncommon  with  frontal  tumours., 
including  pre-frontal  ones.  Tumours  beginning  on  the  under  or 
orbital  surface  of  the  frontal  lobe  may  also  be  associated  with 
early  and  persistent  anosmia  on  the  ipso -lateral  side,  from  im- 
plication of  the  olfactory  bulb  and  tract.  Difficulty  in  moving 
the  head  and  eyes  to  the  contra -lateral  side  would  point  to  a  sub- 
cortical mid-frontal  growth.  Frontal  tumours,  whether  pre-  or 
post-frontal,  are  sometimes  associated  with  a  fine  vibratory 
tremor  of  the  ipso -lateral  arm,  and  less  markedly  of  the  leg,  on 
holding  the  limbs  outstretched^  (though  this  is  far  from  con- 
stant), and  with  loss,  or  speedy  exhaustion,  of  the  contra -lateral 
superficial  reflexes,  especially  the  abdominal  and  epigastric.  If 
the  growth  be  sufficiently  extensive  to  press  backwards  on  the 
pyramidal  tract,  there  may  be  an  increase  in  the  contra -lateral 
deep  reflexes,  with  an  extensor  plantar  reflex  in  the  contra- 
lateral foot,  and  even  a  degree  of  motor  hemi-paresis.  Optic 
neuritis,  generally  late  in  onset,  tends  to  be  more  intense  on 
the  side  of  the  tumour,  whilst  local  tenderness  and  alteration  of 
percussion  note  are  relatively  common.     This  ipso-lateral  papill- 

^  Beevor,  Lettsonian  Lectares,  1907. 

2  Trans.     XIII.    International    Congress :    Section    of    Neuro-pathology, 
p.  239. 

^  Grainger  Stewart,  Lancet,  November  3,  1906. 


470 


NERVOUS    DISEASES 


oedema  of  frontal  lobe  tumours  sometimes  progresses  to  unilateral 
optic  atrophy,  this  latter  occasionally  passing  througli  a  stage  of 
retro-bulbar  neuritis  witb  its  characteristic  central  scotoma. ^ 
In  some  cases,  frontal  tumours  are  associated  with  a  reeling  gait, 
like  that  of  cerebellar  disease  (as  in  the  case  shown  in  Fig.  228). 
Whether  this  is  due  to  backward  displacement  of  the  brain  pro- 
ducing compression  of  the  cerebellum,  or  to  the  transmission  of 


Fig.  228. — Left  pre-frontal  tumour. 

abnormal  impulses  along  the  crossed  fronto-cerebellar  path,  is  at 
present  difficult  of  decision. 

Tumours  of  the  Temporal  Lobe  are  the  most  difficult  of  all 
to  localise,  especially  right-sided  tumours.  This  is  because  their 
symptoms  are  produced  chiefly  by  implication  of  adjacent  parts, 
and  only  to  a  lesser  extent  by  true  focal  lesions.  There  are,  how- 
ever, two  focal  symptoms  which  are  of  diagnostic  value. 

Firstly,  tumours  of  the  tip  of  the  lobe,  in  the  region  of  the 
uncinate  gyrus,  are  often  associated  with  sudden  attacks  commenc- 
ing with  an  olfactory  or  gustatory  sensation,the  smell  being  usually 

1  Foster  Kennedy,  American  Journal  of  Medical  Sciences,  Sept.  191 1. 


INTRA-CRANIAL    TUMOURS  471 

an  unpleasant  one.  This  aura  is  followed  by  a  curious  "  dreamy 
state,"  lasting  several  seconds,  during  which  everything  seems  to 
the  patient  to  be  unreal  or  "  far  away."  These  uncinate  fits  are 
occasionally  accompanied  by  smacking  movements  of  the  Ups. 
They  may  pass  on  directly  to  a  general  epileptiform  fit. 

Secondly,  tumours  of  Heschl's  convolution  (on  the  Sylvian 
surface  of  the  lobe)  and  of  the  adjacent  first  temporal  gyrus,  if 
on  the  left  side,  may  produce  slight" word-deafness  with  par-aphasia, 
&c.  (see  p.  111). 

But  many  temporal  tumours  are  totally  devoid  of  focal  symp- 
toms, and  only  produce  symptoms  of  pressure  on  neighbouring 
parts.  Thus  pressure  on  the  corona  radiata  may  cause  a  shght 
hemiplegia,  or,  more  usually,  a  facio -brachial  monoplegia,  with 
disordered  reflexes  of  the  corresponding  side.  Or  tumours  of  the 
antero -internal  aspect  of  the  lobe  may  impUcate  the  optic  tract, 
or  may  extend  to  the  crus  cerebri,  or  to  the  corpora  quadrigemina, 
producing  corresponding  symptoms. 

Tumours  of  the  Post-central  Convolution. — Here  the  focal 
symptoms  of  a  cortical  growth  consist  of  attacks  commencing 
with  a  sensory  aura  either  of  tingling  or  of  pain  in  the  opposite  face, 
arm,  or  leg,  according  to  the  position  of  the  irritative  lesion.  If 
the  growth  extends  across  the  fissure  of  Rolando  to  the  pre-central 
or  motor  convolution  (or  even  in  many  cases  where  the  pre-central 
convolution  is  not  actually  invaded  but  only  compressed),  there  is, 
in  addition,  a  motor  spasm  of  the  corresponding  part.  Both  in 
cortical  and  in  sub -cortical  tumours  of  the  post-central  convolu- 
tion there  is  usually  anaesthesia,  monoplegic  or  hemiplegic,  and 
of  cortical  or  capsular  type  as  the  case  may  be  (see  p.  208). 
Astereognosis  in  the  contra-lateral  hand  has  also  been  observed. 
Figs.  229  and  229a  show  a  glioma  of  the  left  post-central  gyrus, 
spreading  inwards  to  the  centrum  ovale.  In  this  case  the  initial 
symptoms  were  clumsiness,  loss  of  joint  sense,  and  astereognosis 
of  the  right  hand.  Later,  Jacksonian  convulsions  occurred  in  the 
right  face  and  hand,  and  subsequently  there  was  progressive  right 
hemiplegia  and  hemi-angesthesia  with  aphasia. 

Tumours  of  the  Supra-marginal  and  Angular  Convolutions. 
— General  symptoms  are  usually  late  in  onset.  The  chief  focal 
symptoms  are  due  to  affection  of  the  visual  paths.  In  left-sided 
cases,  implicating  the  angular  gyrus,  word-blindness  may  occur  ; 
in  irritative  lesions  this  is  transitory,  in  destructive  or  sub-cortical 


472 


NERVOUS    DISEASES 


lesions  it  is  permanent.  A  superficial  tumour  limited  to  tlie  angular 
gyrus  may  produce  "  crossed  amblyopia  "  (see  p.  46).  Thus  a 
lesion  of  the  right  angular  gyrus  produces  concentric  contraction 
of  the  visual  field  of  the  left  eye  (see  Fig.  58,  p.  133).  Such  cases 
are  uncommon,  but  have  been  occasionally  recorded.^  More 
usually  the  growth  dips  in  so  as  to  affect  the  underlying  optic 
radiations,  and  then  hemianopia  results  in  the  contra -lateral  half 
of  both  visual  fields.  Hemi-ansesthesia  and  he  mi-analgesia  may 
be  present  in  addition,  when  the  posterior  end  of  the  internal 
capsule  is  affected  ;   motor  hemiplegia  is  uncommon. 


Figs.  229  and  229a. 


Tumours  of  the  Postero-parietal  Lobule  are  sometimes  said 
to  be  characterised  by  astereognosis  in  the  contra -lateral  hand.^  In 
such  cases  the  patient  cannot  recognise  the  form  and  qualities  of 
common  objects  placed  in  his  hand  if  his  eyes  are  closed,  whereas 
with  the  healthy  ipso -lateral  hand  he  recognises  them  at  once. 
But  stereognosis  is  a  complex  intellectual  function,  a  judgment, 
based  on  many  sensory  factors,  and  astereognosis  has  also  been 
observed  in  many  other  conditions,  as  in  disease  of  the  post-central 
gjrrus,  of  the  optic  thalamus,  of  the  posterior  spinal  nerves  and  of 
the  peripheral  sensory  nerves. 

Tumours  of  the  Occipital  Region. — This  area  of  the  brain  is 

1  Beevor,  Lancet,  1907,  p.  719. 

^  Cf.   a  case  by  Edwards  and   Cotterill,  Rev.  of  Neurol,  and  Psychiatry, 
1911,  p.  157. 


INTRA-CRANIAL   TUMOURS  473 

associated  with  the  half -vision  centre.  The  cortical  half -vision 
centre  is  situated  mainly  on  the  mesial  aspect  of  the  occipital  lobe, 
partly  above  and  partly  below  the  calcarine  fissure.  The  lower 
quadrant  of  the  half-field  is  represented  above  the  fissure,  i.e.  in 
the  cuneate  lobule,  the  upper  qua  1  rant  is  below  the  fissure,  i.e. 
in  the  b'ngual  gyrus.  Tumours  of  this  region,  therefore,  produce 
as  their  most  constant  symptom  half -blindness  or  hemianopia, 
which  may  be  complete  or  incomplete  (quadrantic),  according  as 
the  whole  of  the  cortical  centre  is  affected  or  only  part  above  or 
below  the  calcarhie  fissure.  Wernicke's  hemiopic  pupillary  pheno- 
menon (see  p.  !^^  is  absent  in  hemianopia  from  occipital  lesions. 
Tumours  on  the  surface  produce  irritative  phenomena,  whilst  those 
extending  deeper,  into  the  optic  radiations,  produce  paralytic 
symptoms.  The  irritative  phenomena  consist  of  crude  subjective 
visual  hallucinations,  such  as  luminous  sparks  or  flashes  of  light,  in 
the  contra -lateral  halves  of  the  visual  fields  of  both  eyes,  or  in  that 
part  of  the  half-field  corresponding  to  the  area  of  cortex  afiected. 
Such  luminous  sensations  are  usually  followed  by  hemianopia  in 
the  same  area  of  the  visual  field,  a  hemianopia  at  first  transient, 
but  which  may  become  permanent.  Tumours  of  the  cuneate  and 
lingual  gjvi  may  also  press  downwards  on  the  cerebellum,  in 
which  case  cerebellar  phenomena  are  superadded. 

Let  us  now  pass  to  the  consideration  of  tumours  deep  within 
the  substance  of  the  brain.  These  are  more  difficult  to  localise 
than  cortical  growths. 

To  distinguish  between  growths  in  the  Corona  Eadiata  and  those 
in  the  Internal  Capsule  is  often  difficult,  especially  when  the  tumour 
is  a  large  one.  All  that  it  may  be  possible  to  state  is  that  the 
tumour  is  somewhere  in  one  cerebral  hemisphere.  But  with  less 
extensive  growths,  producing  less  complete  hemiplegia,  the  degree 
of  paralysis  of  different  limbs  is  of  diagnostic  value.  Thus  the 
closer  a  lesion  is  situated  to  the  cortex,  the  greater  is  the  tendency 
towards  a  monoplegia.  Also  if  there  be  a  hemiplegia  which  is 
complete  in  the  lower  limb  but  incomplete  in  the  upper,  and  if 
we  find  that  the  hand  is  more  affected  than  the  shoulder,  this 
would  point  to  a  capsular  lesion  rather  than  a  sub -cortical  one, 
since  in  the  cortex  the  shoulder  centre  is  the  one  nearest  to  that 
for  the  lower  limb  (see  Figs.  .3  and  7). 

Tumours  of  the  Central  Gang-lia. — In  this  region  growths  may 
develop   without   producing   enough   focal    symptoms    to    render 


474  NERVOUS   DISEASES 

localisation  possible.  From  the  close  proximity  of  the  optic 
thalamus  and  corpus  striatum  to  the  motor,  sensory,  and  visual 
paths  in  the  internal  capsule,  a  slowly  progressive  hemi-paresis 
or  hemiplegia  may  occur,  accompanied  by  hemianopia  and  a 
degree  of  hemi-ansesthesia.  But  if  these  phenomena  be  present, 
say  on  the  right  side,  and  nothing  more,  beyond  the  general  signs 
of  intra-cranial  tumour,  all  that  we  can  diagnose  is  a  growth  some- 
where within  the  left  cerebral  hemisphere,  and  probably  in  its 
posterior  two-thirds.  But  sometimes  we  can  be  more  precise. 
For  example,  Nothnagel  long  ago  showed  that  the  optic  thalamus 
is  a  lower  reflex  centre  for  the  emotional  movements  of  laughing 
and  crying,  and  cases  of  thalamic  lesion  have  been  demonstrated 
in  which  voluntary  movements  of  the  face  were  preserved  whilst 
emotional  movements  were  impaired  or  lost  on  the  contra-lateral 
side  of  the  face.  Further,  a  small  lesion  in  the  lower  and  posterior 
part  of  the  thalamus  may  cause  (probably  from  affection  of  the 
adjacent  rubro -spinal  path)  spontaneous  slow  rhythmic  move- 
ments of  the  contra -lateral  limbs,  athetoid  or  choreiform,  increased 
on  voluntary  exertion.  The  plantar  reflex  in  these  cases  remains 
flexor  in  type,  provided  the  internal  capsule  be  not  involved. 
Again,  the  optic  thalamus  is,  as  we  have  already  seen,  an  important 
station  in  the  general  sensory  path,  and  therefore  sensory  symptoms 
are  sometimes  prominent,  especially  subjective  sensations  of  pain, 
heat,  and  cold,  in  the  contra -lateral  side  of  the  body,  together  with 
a  degree  of  hemi-ansesthesia.  Many  cases  of  thalamic  tumour,  how- 
ever, run  their  course  without  any  sensory  impairment  whatever. 
Tumours  of  the  Corpus  Callosum  have  no  focal  symptoms 
which  can  be  regarded  as  pathognomonic.  Tumours  in  the  anterior 
part  of  this  great  commissure  generally  produce  early  mental 
symptoms  resembhng  those  of  paralytic  dementia.  To  these  may 
be  superadded  unilateral  or  bilateral  hemi-paresis  or  convulsions, 
(cranial-nerve  palsies,  as  a  rule,  being  absent).  But  these  motor 
symptoms  are  probably  the  result  of  extension  into  neighbouring 
parts,  so  that  to  diagnose  a  callosal  growth  is  always  hazardous. 
Moreover,  it  is  rare  for  a  tumour  to  be  limited  to  the  corpus 
callosum  without  extension  into  one  or  both  hemispheres.  Atten- 
tion has  been  drawn  ^  to  the  occurrence,  without  hemiplegia,  of  left- 
sided  motor  apraxia  (inabihty  to  perform  certain  movements  when 

^  Wilson,    Brain,    1908,  p.    164;  also   Lippmann,  Archiv.  fur   Psychiatrie, 
1908,  xliii. 


INTRA-CRANIAL    TUMOURS  475 

there  is  no  actual  paralysis  of  the  limb)  in  callosal  lesions.  (See 
p.  116). 

Marchiafava  ^  has  described  a  peculiar  degeneration  of  certain 
commissural  tracts  of  the  corpus  callosum  in  chronic  alcoholism. 

Tumours  of  the  Corpora  Quadrigemina  (and  of  the  Pineal 
Body  which  lies  in  close  apposition)  are  localised  with  comparative 
ease  by  the  presence  of  characteristic  ocular  phenomena.  These 
consist  in  a  paralytic  affection  of  the  third  nerve  nuclei,  more  or 
less  symmetrically  on  the  two  sides.  The  commonest  sign  is  a  com- 
bination of  bilateral  ptosis  with  weakness  of  upward  and  downward 
movements  of  the  eyes  and  feebleness  of  convergence.  The 
pupillary  reflex  may  be  sluggish  or  absent.  Certain  tumours, 
especially  teratomata  of  the  pineal  gland,  occurring  in  children, 
are  associated  with  what  has  been  called  nmcrogenitosoniia,  consist- 
ing in  excessive  growth  of  the  body,  precocious  sexual  develop- 
ment and  abnormal  growth  of  the  penis  and  pubic  hairs,  also  wath 
mental  and  vocal  precocity.  (These  signs  are  in  addition  to  the 
ocular  phenomena  above  described.)  In  this  respect  they  contrast, 
as  we  shall  presently  see,  with  certain  tumours  of  the  pituitary  body 
in  which  the  genital  functions  may  be  diminished.  Less  constantly, 
in  unilateral  quadrigeminal  disease,  a  degree  of  deafness  has  been 
noted  in  the  ear  of  the  opposite  side,  the  sub-cortical  auditory 
centre  being  located  in  the  posterior  corpus  quadrigeminum.  If 
the  superior  cerebellar  peduncle,  which  is  in  close  proximity,  be 
also  implicated,  we  have  a  corresponding  cerebellar  asynergia  or 
ataxia  and  reeling  gait,  whilst  if  the  adjacent  external  geniculate 
body  or  optic  radiations  be  involved,  there  is  hemianopia. 

Tumours  of  the  Tegmental  Region  of  the  Crus  or  Pons 
produce  characteristic  focal  symptoms  from  implication  of  the  rubro- 
spinal tract  (Monakow's  bundle)  which  starts  from  the  red  nucleus, 
runs  down  in  the  pons,  crosses  the  middle  line  and  traverses  the 
antero -lateral  column  on  the  opposite  side  of  the  spinal  cord. 
Lesions  in  the  crural  or  pontine  part  of  this  tract  produce  a  slow 
rhythmic  tremor  of  the  contra-lateral  hand  and  foot,  somewhat 
like  that  of  paralysis  agitans,  increased  by  voluntary  exertion  or 
excitement  and  ceasing  during  sleep.  If  the  lesion  be  in  the  red 
nucleus  itself,  which  is  transfixed  by  the  fibres  of  the  third  nerve, 
we  have,  in  addition,  third-nerve  palsy  of  the  ipso -lateral  side 
with  tremor  of    the    contra -lateral    arm   and   leg  —  a    condition 

1  Rendie  delta  R.  Accad,  de.i  Lincei,  1910,  xiv.,  series  5,  fasc.  3. 


476  NERVOUS    DISEASES 

known  as  "  Benedikt's  syndrome."  If  the  growth  implicates 
the  sensory  tract  of  the  fillet,  there  may  be  hemi-anaesthesia  of 
the  contra -lateral  side  of  the  body,  but  this  is  less  common  with 
tumours  than  with  sudden  vascular  lesions  such  as  haemorrhage,  &c. 

A  Tumour  of  the  Crusta  or  Ventral  Region  of  the  Crus 
Cerebri  is  easy  of  recognition,  from  the  characteristic  alternate  par- 
alysis which  is  produced,  consisting  in  third-nerve  palsy,  generally 
incomplete,  on  the  ipso-lateral  side,  with  hemiplegia  of  the  contra- 
lateral face,  arm,  and  leg — "  Weber's  syndrome  "  (see  Fig.  99, 
p.  236).  As  the  tumour  increases  in  size,  it  tends  to  cross  the 
middle  line  and  implicate  the  opposite  third  nerve  as  well. 

Pituitary  Tumours  produce  diagnostic  symptoms  in  two 
entirely  different  ways.  Firstly,  we  may  have  signs  of  disordered 
activity  of  the  pituitary  gland  itseK  (dys-pituitarism),  and  especially 
of  its  anterior  lobe.  Excessive  activity  of  the  gland  {super- 
fituitarism)  influences  the  growth  of  the  bones  throughout  the  body, 
producing  acromegaly  or  gigantism  (according  to  whether  the 
epiphyseal  cartilages  have  become  ossified  or  not).  But  skeletal 
changes  are  not  constant.  They  seem  to  occur  chiefly  in  cases  of 
adenomatous  growth,  accompanied  by  hyper-activity  of  the  anterior 
lobe  of  the  gland,  and  not  in  purely  destructive  lesions  as  in  the 
sarcomata. 

Diminished  activity  [sub-fituitarism),  on  the  other  hand,  pro- 
duces the  so-called  adiposo-genital  dystrophy  (Frohlich's  syndrome), 
evidenced  by  an  excessive  deposit  of  fat  throughout  the  body 
(see  Fig.  230),  together  with  absence  of  sexual  development  if  the 
process  dates  from  childhood,  or  regression  from  sexual  maturity 
if  the  disease  appears  in  adult  life.  Thus  in  female  patients  we 
observe  amenorrhoea,  whilst  an  adult  male  patient  develops  a 
remarkable  tendency  to  approximate  to  a  female  type ;  the  mam- 
mary glands  enlarge,  the  testicles  diminish  in  size,  the  abdomen 
becomes  rounded  like  a  woman's,  and  the  pubic  hair  becomes 
restricted  in  area — "  pituitary  eunuchism,"  ^  accompanied  by  loss 
of  virility.  There  is  also  an  abnormal  sugar-tolerance,  so  that  the 
patient  can  take  an  excessive  amount  of  glucose  without  showing 
glycosuria. 

Ateleiosis  or  pituitary  infantilism,  a  peculiar  variety  of  arrested 
growth  without  adiposity,  is  also  due  to  sub-pituitarism.  The 
ateleiotic  dwarf  has  a  childish  facies,  a  dehcate,  soft  skin,   and 

^  Nonne,  Neurologisches  Oentralblatt,  1907,  s.  735. 


INTRA-CRANIAL    TUMOURS 


477 


thin  piping  voice.     His  long  bones  are  small  and  fine,  and  their 
epiphyses  are  not  united.     The  teeth  are  incompletely   erupted. 


Fig.  230. — Adiposo-genital  dystrophy  in  a  boy  of  fourteen.  He  also  had  ex- 
cessive sugar-tolerance  and  was  able  to  take  300  grammes  of  glucose  with- 
out inducing  glycosuria. 

The  pulse  is  slow  and  the  arterial  pressure  low.     Ateleiosis,  as 
Hastings  Gilford  has  shown,  may  begin  during  foetal  life,  during 


478  NERVOUS    DISEASES 

infancy  or  early  childhood,  or  at  any  time  before  puberty.  The 
ateleiotic  patient  retains  throughout  life  the  physical  characters 
of  his  age  at  the  time  when  his  symptoms  first  developed.  If  the 
disease  begins  in  infancy,  the  fontanelle  may  remain  open  for 
years.  If  it  commences  during  foetal  life,  the  testicles  remain 
undescended  and  the  sexual  organs  rudimentary. 

Sub-pituitarism  may  occur  as  a  primary  disease,  or  it  may 
supervene  after  a  previous  stage  of  super-pituitarism  and  giant 
growth.  We  rarely  meet  with  pure  super-pituitarism  or  pure 
sub-pituitarism  ;  both  types  of  dys-pituitarism  are  usually  inter- 
mingled, in  varying  proportions. 

Secondly,  and  more  constantly,  in  pituitary  tumours  there  are 
focal  symptoms  produced  by  pressure  on  adjacent  parts,  notably  on 
the  optic  chiasma.  Bi-temporal  hemianopia,  with  a  hemiopic  pupil- 
reaction,  results.  This  may  afterwards  progress  to  total  blindness 
of  one  eye  with  temporal  hemianopia  of  the  other  (see  p.  133).  In 
pituitary  tumours  primary  optic  atrophy  is  commoner  than  optic 
neuritis.  A  growth  in  the  pituitary  gland  may  also  press  back- 
wards on  the  third  nerves,  causing  ocular  palsies,  or  it  may 
extend  upwards  towards  the  floor  of  the  third  ventricle,  in  which 
case  we  sometimes  note  persistent  somnolence  (see  Figs.  225  and 
225a),  or  it  may  press  upwards  against  the  uncinate  lobe,  causing 
uncinate  fits,  or  upon  the  frontal  lobe,  producing  mental  dulness, 
&c.  The  diagnosis  of  pituitary  tumour  can  often  be  confirmed 
by  radiography,  showing  deepening  of  the  sella  turcica.  Glyco- 
suria is  not  uncommon  in  super-pituitarism. 

Tumours  of  the  Cerebellum  and  Cerebellar  Peduncles. — The 
anatomical  connections  of  the  cerebellum  are  all-important,  and 
should  be  carefully  borne  in  mind  (see  pp.  23  to  31).  Of  all  intra- 
cranial tumours,  those  of  the  cerebellum  are  the  most  frequent. 
Intra -cerebellar  growths  are  usually  tuberculous  or  gliomatous, 
whereas  extra -cerebellar  growths,  commonly  situated  in  the  ponto- 
cerebellar angle  of  the  posterior  fossa,  if  arising  from  the  ventral 
surface  of  the  cerebellum,  are  generally  gliomata,  and  if  arising 
from  the  sheaths  of  cranial  nerves  (especially  the  auditory  nerve) 
they  are  most  commonly  fibro-myxomata. 

Vertigo,  a  reehng  gait,  uninfluenced  by  closure  of  the  eyes, 
nystagmus,  and  early  optic  neuritis  are  the  outstanding  symptoms 
common  to  growths  in  the  region  of  the  cerebellum,  but  a  closer 
study  usually  enables  us  to  localise  the  lesion  more  exactly. 


INTRA-CRANIAL    TUMOURS  479 

In  cerebellar  disease  we  have  to  distinguish  not  only  between 
affections  of  the  vermis  and  of  the  lateral  lobes,  but  also  between 
affections  of  the  cerebellar  cortex  and  of  the  intra-cerebellar  nuclei. 
Many  tumours  and  abscesses  implicate  cortex  and  nuclei  together, 
and  in  such  cases  we  have  a  combination  of  cortical  and  sub-cortical 
phenomena. 

Tumours  of  the  middle  lobe  or  vermis  are  associated  with  the 
typical  cerebellar  gait.  There  is  also  a  tendency  to  fall  forwards  or 
backwards,  according  as  the  lesion  is  situated  in  the  anterior  or 
posterior  part  of  the  vermis.  There  is  often  a  tendency  for  the  head 
to  fall  backwards  or  forwards,  and  not  uncommonly  the  movements 
of  the  head  and  of  the  facial  muscles  are  curiously  slow  and  clumsy. 
Asynergia  and  hypermetria  are  present  in  all  the  limbs,  but  without 
unilateral  preponderance  on  either  side,  until  the  growth  extends 
into  one  or  other  lateral  lobe. 

Tumours  of  the  cerebellar  cortex  of  the  lateral  lobe  produce 
unilateral  symptoms  in  the  ipso-lateral  limbs,  consisting  in  dys- 
diadocokinesia  (see  Cerebellar  Ataxia,  p.  276),  hemi-asynergia,  and 
hypermetria.  On  making  the  patient  stand  in  turn  on  each  foot 
separately,  we  find  that  he  tends  to  stand  less  securely  on  the  leg 
of  the  ipso-lateral  side.  In  walking,  he  lurches  and  reels,  sometimes 
towards  the  side  of  the  lesion,  sometimes  away  from  it.  In  addi- 
tion we  find  spontaneous  deviation  in  the  ipso-lateral  limbs  with 
Barany's  pointing-tests  (see  p.  29),  together  with  loss  of  the  normal 
deviation  of  the  ipso-lateral  limb  on  inducing  a  temporary  vesti- 
bular nystagmus. 

Disease  implicating  the  sub-cortical  or  intra-cerebellar  nuclei 
produces  marked  unsteadiness  of  the  limbs  with  a  tendency  to  fall 
towards  the  affected  side.  In  cases  imphcating  the  fibres  of  the 
middle  cerebellar  peduncle  this  may  be  so  marked  that,  even  when 
lying  down,  the  patient  may  tend  to  roll  out  of  bed  towards  the 
affected  side — so-called  forced  rotatory  movements,  around  the  long 
axis  of  the  body,  analogous  to  those  produced  by  experimental 
stimulation  (see  p.  62).  Thus  in  one  case  of  my  own,  where  there 
was  a  large  sarcoma  within  the  right  lateral  lobe,  the  patient  rolled 
persistently  towards  his  right  side,  and  occasionally  feU  over  the 
right  edge  of  his  bed.  Unfortunately  the  direction  of  rotation  is 
not  sufficiently  constant  to  be  of  diagnostic  value  in  determining 
the  side  of  the  lesion,  but  when  the  phenomenon  occurs,  it  is  a 
valuable  corroborative  sign  of  disease  of  the  middle  peduncle. 


480  NERVOUS    DISEASES 

"  Cerebellar  catalepsy,"  and  the  rare  cases  of  "  cerebellar 
fits,"  tonic  in  type,  are  also  indicative  of  disease  of  the  sub- 
cortical nuclei. 

Nystagmus,  which  was  formerly  included  amongst  the  cardinal 
signs  of  cerebellar  disease,  also  the  occasional  shew-deviation  of  the 
eyes,  are  now  considered  to  be  due,  not  to  pure  cerebellar  affection, 
but  to  disease  of  the  adjacent  Deiters'  nucleus  or  its  connections. 
The  nystagmus  is  horizontal  in  type,  its  coarser  phase  occurring 
on  looking  towards  the  ipso-lateral  side.  Together  with  this,  there 
is  often  weakness  of  conjugate  movement  of  the  eyes  towards  the 
side  of  the  lesion. 

The  subjective  vertigo,  so  frequently  present  in  cases  of  cere- 
bellar tumour,  in  which  surrounding  objects  appear  as  if  rotating 
towards  the  contra-lateral  side,  is  probably  due  to  affection  of  the 
adjacent  vestibular  nuclei  or  their  connections.  So  also  the  occa- 
sional curious  attitude  of  the  head  (see  Fig.  150,  p.  308)  is  due  to 
vestibular  and  not  to  primary  cerebellar  disease. 

The  condition  of  the  deep  reflexes  is  inconstant.  Pure  cerebellar 
disease,  which  leaves  the  long  sensory  and  motor  tracts  in  the  brain- 
stem unaffected,  produces  neither  sensory  loss,  motor  paralysis, 
nor  alteration  of  reflexes.  Sometimes,  however,  by  pressure,  or  by 
infiltration,  one  or  both  pyramidal  tracts  may  become  implicated, 
in  which  case  may  be  superadded  the  characteristic  increase  of  deep 
reflexes  on  one  or  both  sides,  with  extensor  plantar  responses. 

Extra-cerebellar  tumours  most  frequently  arise  in  the  ponto- 
cerebellar angle,  and,  as  a  rule,  are  not  difficult  of  recognition. 
Most  of  them  arise  from  the  sheath  of  the  auditory  nerve.  Some- 
times they  are  bilateral,  as  in  Fig.  231.  The  focal  symptoms  are, 
first  of  all,  those  of  auditory  affection,  consisting  in  progressive 
nerve-deafness,  often  preceded  or  accompanied  by  tinnitus  in  the 
corresponding  ear.  There  is  also  vestibular  affection,  with  vertigo  ^ 
and  impairment  of  thermic  nystagmus  and  of  other  vestibular 
reactions  (see  p.   160).     To  these  signs  is  frequently  superadded 

^  The  direction  of  subjective  rotation  may  be  compared  with  the  ap- 
parent rotation  of  outside  objects.  In  some  intra-cerebellar  cases  the 
direction  of  the  subjective  sense  of  rotation  felt  by  the  patient  is  the  same 
as  that  of  apparent  rotation  of  external  objects,  viz.  towards  the  contra- 
lateral side.  In  extra-cerebellar  cases  these  two  are  sometimes  opposed, 
so  that  the  patient  may  have  a  subjective  sensation  of  rotation  towards 
the  ipso-lateral  side.  This  alleged  difference  between  intra-  and  extra-cere- 
bellar tumours  as  regards  subjective  sense  of  rotation  is  doubted  by  Oppen- 
heim  and  by  other  competent  observers.  It  is  therefore  too  uncertain  to 
be  conclusive,  by  itself. 


INTRA-CRANIAL    TUMOURS 


481 


paresis  of  the  adjacent  facial  nerve — a  sign  of  great  value  when 
present.  Later,  a  vestibular  attitude  of  the  head  may  develop 
and,  with  or  without  this,  signs  of  ipso-lateral  cerebellar  dis- 
ease, cortical  and  nuclear,  appear.  Further,  by  extension  of  the 
tumour  forwards  towards  the  pons,  or  downwards  towards  the 
medulla.,  other  cranial  nerves  may  become  affected  on  the  side  of 


Fig.  231. — Bilateral  auditory-nerve  tumours  (A  and  B)  in  ponto-cerebellar  angles. 
An  attempt  was  made  to  remove  the  larger  tumour  (B)  by  operation,  hence 
the  laceration  of  the  corresponding  lateral  lobe  of  the  cerebellum. 


the  tumour,  especially  the  fifth  and  sixth  nerves.  The  trigeminal 
nerve  may  show  irritative  changes  in  the  form  of  neuralgic  pains, 
and,  more  constantly,  paralytic  changes,  usually  moderate  in 
degree,  evidenced  by  diminution  of  sensation  in  the  trigeminal 
area.  One  of  the  earhest  phenomena  of  trigeminal  paresis  consists 
in  loss  of  the  corneal  reflex  on  the  ipso-lateral  side.  Later  on,  from 
affection  of  the  pyramidal  tract  in  the  brain-stem,  we  may  have 
hemiplegic  symptoms,  generally  slight  in  degree,  on  one  or  other 

2h 


482 


NERVOUS    DISEASES 


side,  more  commonly  in  the  ipso-lateral  limbs,  probably  due  to 
pressure  of  the  brain-stem  against  the  opposite  bony  wall  of  the 
skull. 

Tumours  of  the  Pons. — In  this  region  focal  symptoms  usually 
appear  early,  but  general  symptoms,  especially  optic  neuritis, 
tend  to  be  late  in  onset.  The  most  characteristic  sign  of  a  uni- 
lateral pontine  lesion  is  an  "  alternate  "  paralysis  of  the  fifth, 
sixth,  or  seventh  cranial  nerve  or  nucleus  on  the  ipso-lateral 
side,  together  with  hemiplegia  of  the  contra-lateral  arm  and  leg 
and  an  extensor  plantar  response,  or,  if  the  growth  be  situated  in 


Fig.  232. — Sarcoma  occupying  centre  of  pons. 

the  dorsal  region  of  the  pons,  there  may  be  hemi-anaesthesia  of  the 
contra-lateral  side  of  the  body.  If  the  lesion  infiltrates  the  ponto- 
cerebellar angle,  internal  to  the  point  of  emergence  of  the  auditory 
nerve,  there  may  be  hemi-analgesia  and  hemi-thermansesthesia 
from  implication  of  the  fibres  for  pain  and  temperature,  which  at 
this  level  are  at  some  Httle  distance  from  the  path  for  tactile  sen- 
sation (see  Fig.  12,  p.  18).  According  as  the  growth  is  primarily 
intra-pontine  or  extra-pontine  in  origin,  the  affection  of  cranial 
nerves  will  be  primarily  nuclear  or  infra-nuclear  in  type,  and 
the  grouping  of  the  symptoms  will  be  slightly  different.  We 
have  already  studied  the  differences  between  a  nuclear  and  an 
infra -nuclear  affection  of  the  sixth  and  seventh  nerves  (see  pp.  149 


INTRACRANIAL    TUMOURS  483 

and  160).  Tumours  of  the  auditory  nerve  are  relatively  common, 
and  often  bilateral ;  they  ultimately  produce  signs  of  extra-cere- 
bellar  growth,  as  we  have  seen  (p.  480). 

The  clinical  picture  of  alternate  paralysis  is  often  masked  by 
the  fact  that  pontine  tumours  rarely  remain  confined  to  one  side, 
but  tend  to  spread  bilaterally.  In  such  cases  we  depend  for  our 
diagnosis  on  the  existence  of  nuclear  or  infra -nuclear  paralysis 
of  the  fifth,  sixth,  and  seventh  nerves,  together  with  signs  of 
implication  of  the  motor  or  sensory  tracts  or  of  the  cerebellar 
peduncles. 

Tumours  of  the  Medulla  Oblongata. — In  this  region  the  chief 
diagnostic  feature  is  paralysis,  unilateral  or  bilateral,  of  the  lowest 
cranial  nerves,  from  the  ninth  to  the  twelfth,  producing  disorders  of 
articulation,  deglutition,  &c.,  together  with  signs  of  interruption 
of  the  afferent  or  efferent  tracts  coursing  through  the  medulla. 

Tumours  of  the  Fourth  Ventricle  may  arise  either  from  the 
ependyma,  or  from  the  choroid  plexus,  or  they  may  be  parasitic 
cysts  caused  by  cysticerci.  In  such  ventricular  growths  focal 
symptoms  may  be  absent.  If,  however,  the  lesion  extends  into 
the  dorsal  part  of  the  pons  or  medulla,  or  into  the  cerebellum, 
corresponding  symptoms  develop.  Glycosuria  is  relatively  com- 
mon. We  have  already  referred  to  the  pecuUar  form  of  vertigo 
which  occurs  in  cases  of  free  cysticercus  in  the  ventricle  (p.  169). 

Pathological  Diagnosis  of  Intracranial  Growths. — In  any 
given  case  it  may  be  impossible  to  diagnose  with  certainty  the  nature 
of  the  growth,  since  the  symptoms  depend  not  on  the  structure 
but  on  the  anatomical  position  of  the  tumour.  But  if  there  is  a 
history  of  syphihs,  and  still  more  if  the  Wassermann  reaction  in 
the  blood-serum  is  positive,  a  gumma  may  be  suspected,  and  the 
patient  should  be  given  the  benefit  of  energetic  anti-syphilitic 
treatment  for  a  time.  Noguchi's  luetin  reaction  in  the  skin, 
when  a  dead  culture  of  several  strains  of  treponema  pallidum  is 
injected  hypodermically,  is  an  important  method  of  diagnosing 
latent  syphihs.  In  a  syphilitic  individual  the  luetin  injection  pro- 
duces a  reddish  indurated  papule  or  pustule,  often  surrounded  by 
an  inflammatory  area  and  lasting  four  or  five  days.  It  must  not 
be  forgotten,  however,  that  even  gummata  sometimes  resist  medi- 
cinal treatment,  and  it  may  be  necessary  to  remove  a  cerebral 
syphiloma  by  operation.  Syphilitic  lesions  of  the  central  nervous 
system  are  often  associated  with  an  excess  of  lymphocytes,  together 


484  NERVOUS    DISEASES 

with  the  presence  of  globulin  and  a  positive  Wassermann  reaction, 
in  the  cerebro- spinal  fluid ;  a  normal  fluid  would,  therefore,  be 
against  a  diagnosis  of  syphiloma.  But  an  excess  of  lymphocytes 
occurs  not  only  in  tuberculous  tumours,  but  even  in  true  neoplasms. 
A  sudden  apoplectiform  aggravation  of  the  symptoms  is  suggestive 
either  of  glioma  or  of  aneurism,  gliomata  being,  from  their  loose 
texture  and  high  vascularity,  particularly  liable  to  spontaneous 
haemorrhages.  Aneurisms  sometimes,  and  arterio -venous  aneurisms 
more  often,  may  be  accompanied  by  pulsating  bruits ;  these  may 
not  only  be  perceptible  by  the  patient,  but  can  sometimes  be 
auscultated  by  the  physician. 

Tuberose  sclerosis  is  a  rare  congenital  disease  in  which  there 
are  curious  neoplasms  in  the  brain,  and  frequently  also  in  other 
organs,  notably  the  kidneys,  heart,  and  skin.  The  brain  tumours, 
which  are  often  multiple,  consist  of  an  intermingling  of  "  dislocated  " 
nerve- cells  with  gliomatous  overgrowth.  Sometimes  these  give 
rise  to  the  general  signs  of  intra- cranial  pressure — headache,  optic 
neuritis,  general  convulsions,  &c.  Local  signs  and  symptoms  are 
rare.  The  child  is  usually  epileptic  and  mentally  deficient.  The 
chief  diagnostic  feature  is  the  frequent  presence  of  so-called  sebaceous 
adenomata,  small,  closely-set  tumours  of  the  skin,  disposed  sym- 
metrically on  the  face,  chiefly  about  the  forehead,  bridge  of  the 
nose,  naso-labial  folds,  and  chin  ;  sometimes  also  on  the  skin  of 
the  trunk. 

Cerebral  abscesses  are  mostly  secondary  to  local  infection, 
especially  from  the  middle  ear  or  other  accessory  air-sinuses  (frontal, 
ethmoidal,  or  sphenoidal),  or  they  may  follow  compound  fractures 
of  the  skull,  sometimes  after  an  interval  of  months,  during  which 
the  patient  appears  to  be  healthy  ;  less  commonly  we  find  meta- 
static abscesses  without  local  infection  in  the  head,  e.g.  in  pyaemia, 
ulcerative  endocarditis,  actinomycosis,  and  in  some  cases  of 
bronchectasis,  hepatic  abscess,  &c. 

Brain  abscesses  secondary  to  otitis  media  generally  follow  cases 
of  chronic  rather  than  of  acute  suppuration  of  the  middle-ear, 
although  this  rule  is  not  invariable.  Their  commonest  situation 
is  either  in  the  temporal  lobe  of  the  cerebrum  or  in  the  lateral  lobe 
of  the  cerebellum.  In  either  of  these  situations  an  abscess  produces 
signs  of  general  intra-cranial  pressure,  such  as  headache,  vomiting, 
mental  dulness,  and,  later,  optic  neuritis.  The  pulse  in  brain 
abscess  is  often  specially  slow  (50  to  40  per  minute),  and  the  tem- 


INTEA-CRANIAL    TUMOURS  485 

perature  may  be  normal  or  subnormal.  Once  the  abscess  bursts 
into  the  ventricles  or  into  the  subarachnoid  space,  causing  a  ful- 
minating purulent  meningitis,  the  pulse  and  temperature  at  once 
run  up,  and  the  patient  dies.  A  pysemic  temperature,  with  rigors 
and  acute  fever  of  remittent  type,  occurs  when  infective  thrombosis 
of  the  lateral  sinus  or  other  venous  sinuses  occurs. 

A  temporal  abscess  is  easier  to  recognise  when  left-sided,  owing 
to  the  fact  that  in  right-handed  people  the  left  temporal  lobe 
contains  centres  for  word-hearing  :  hence  in  a  left-sided  temporal 
abscess  the  patient  tends  to  have  par-aphasia  and  makes  mistakes 
in  naming  objects  (see  p.  111).  If  the  abscess  be  large  in  size,  it 
may  press  inwards  towards  the  corona  radiata  and  cause  a  facio- 
brachial  monoplegia,  with  perhaps  loss  of  the  abdominal  reflex 
upon  the  hemiplegic  side.  Further,  by  pressure  backwards  towards 
the  angular  gyrus,  it  may  produce  hemianopia  and,  in  left-sided 
abscesses,  word-blindness.  Or  from  extension  downwards,  towards 
the  floor  of  the  skull  and  the  ocular  nerves,  we  may  have  dilata- 
tion of  the  ipsolateral  pupil,  and  ptosis  or  other  impairment  of 
external  ocular  movements.  Cerebellar  abscess  tends  to  cause 
vertigo,  ataxia  of  ipsolateral  limbs,  with  spontaneous  mispointing 
on  Bariiny's  pointing-tests,  and  nystagmus.  The  patient  often 
lies  habitually  upon  the  healthy  side  of  the  head,  keeping  the  side 
of  the  abscess  uppermost.  Frontal  abscess  commonly  arises  as  a 
direct  result  of  infection  from  the  frontal,  ethmoidal,  or  sphenoidal 
air-sinuses.  The  focal  diagnosis  is  often  difficult,  and  we  must 
be  on  the  look-out  for  special  mental  dulness,  loss  of  the  contra- 
lateral abdominal  reflex,  and  the  presence  of  an  extensor  plantar 
reflex  on  the  corresponding  side. 

Tuberculous  growths  are  specially  common  in  the  pons  and 
cerebellum,  and  the  existence  of  tuberculous  disease  of  the  lungs, 
abdominal  viscera,  or  elsewhere,  would  tend  to  suggest  a  similar 
cause  for  the  intra -cranial  mischief,  particularly  if  the  patient  be 
a  child  or  young  adult.  Calmette's  ophthalmo-reaction  by  inocu- 
lating the  conjunctiva,  or  Von  Pirquet's  cuti-reaction  by  inocu- 
lating the  skin  with  a  solution  of  tuberculin,  are  sometimes  of 
value  in  such  cases. 

Symptoms  of  cerebral  tumour  supervening  in  a  patient  who  has 
already  had  a  malignant  tumour  elsewhere  in  the  body  suggest 
that  the  cerebral  mischief  is  metastatic  in  nature.  In  such  cases 
a  curative  operation  is  out  of  the  question,  since  it  is  probable  that 


486  NERVOUS    DISEASES 

other  tumours  will  be  present,  besides  the  one  which  has  been 
diagnosed. 

Finally,  we  have  to  bear  in  mind  certain  cases  of  pseudo-tumor 
cerebri,  which  may  be  divided  into  four  groups  : — (1)  Cases  which 
after  showing  the  classical  signs  of  brain  tumour  recover  completely 
or  in  which  an  autopsy  shows  no  lesion  capable  of  accounting  for 
the  symptoms.  (2)  Cases  of  acute  hydrocephalus  or  serous  menin- 
gitis of  the  ventricles  (ependymitis),  relieved  by  thecal  puncture. 
Some  of  these  cases  are  associated  with  otitis  media,  in  which  the 
focus  of  suppuration  is  outside  the  dura  mater,  and  the  toxins, 
but  not  the  organisms,  penetrate  the  barrier  and  set  up  a  serous 
meningitis,  in  which  the  cerebro- spinal  fluid  is  sterile  and  may  even 
be  free  from  pleocytosis.  Other  cases  arise  in  the  course  of  general 
fevers,  especially  measles,  influenza,  pneumonia,  enteric  fever,  &c. 
Others,  again,  are  due  to  chronic  lead  poisoning.  Sunstroke  can 
also  produce  an  acute  meningeal  reaction.  (3)  Localised  ependy- 
mitis of  the  Sylvian  aqueduct,  producing  blocking  of  this  canal 
with  enormous  distension  of  the  ventricles.  (4)  Extensive  and 
acute  softenings,  with  headache,  choked  discs,  and  hyper-tension 
of  the  cerebro -spinal  fluid. 

As  a  rule,  however,  pseudo-tumor  is  more  rapid  in  its  evolution, 
and  the  optic  and  ocular  phenomena  appear  early  and  soon  attain 
a  maximum. 


CHAPTER   XXVI 

ORGANIC   WAR-LESIONS    OF   THE   NERVOUS   SYSTEM 

The  advisability  of  considering  war-injuries  in  a  special  category 
is  not  merely  because  of  the  dramatic  buman  interest  aroused  by 
everything  connected  with  the  titanic  European  struggle.  From 
the  niedical  and  scientific  point  of  view  also,  there  are  important 
differences  between  the  injuries  of  war  and  the  diseases  and  acci- 
dents of  peace. 

Firstly,  missiles  which  traverse  the  tissues  produce  effects 
wholly  different  from  those  which  result  from  spontaneous  morbid 
processes.  They  damage  indiscriminately  anatomical  structures 
which  are  seldom  simultaneously  affected  in  disease.  Moreover, 
when  focal  lesions  similar  to  the  war-injuries  of  healthy  brains  do 
occur  spontaneously  from  disease,  they  are  the  result  of  pre-existing 
morbid  processes,  which  arise  either  in  the  nervous  tissues  them- 
selves, or,  more  commonly,  in  the  blood-vessels  or  meninges. 
Further,  war-injuries  produce  their  effects  not  so  much  from  the  mere 
mechanical  damage  of  the  projectile  as  by  the  inward  penetration 
of  infective  organisms.  In  wounds  of  the  nervous  system  which 
are  not  immediately  fatal,  the  chances  of  recovery  largely  depend 
on  whether  septic  infection  is  present  or  not. 

Focal  lesions  from  war-injuries  in  healthy  young  brains  and 
spinal  cords,  if  aseptic,  are  practically  equivalent  to  physiological 
experiments,  and  the  syndromes  which  result  are  different  from 
those  which  occur  in  the  course  of  disease. 

Lastly,  owing  to  the  healthy  condition  of  the  tissues  originally 
damaged,  the  prospects  of  recovery  after  war-lesions  of  the  nervous 
system  are  much  greater  than  can  be  expected  after  lesions  which 
result  from  disease. 

Brain  Wounds 

The  brain  is  protected  against  injuries  from  without  by 
several  hues  of  defence.  Firstly  there  is  the  thick  scalp, 
separated  by  loose  connective  tissue  from  the  skull.      This   has 

487 


488  NERVOUS   DISEASES 

its  pericranium  outside,  for  the  nourishment  and  repair  of  the 
outer  table.  The  dense  outer  table  is  separated  from  the  dense 
inner  table  by  the  spongy  diploe,  and  sometimes  by  air-sinuses. 
Where  the  diploe  is  absent  and  the  outer  and  inner  tables  are  in 
apposition,  as  in  the  temporal  and  sub-occipital  regions,  additional 
protection  is  afforded  by  the  superjacent  temporal  and  cervical 
muscles.  Close  within  the  skull  is  the  dura  mater,  tough  and  strong. 
This  acts  as  an  internal  periosteum  to  the  inner  table.  It  is  also 
an  important  mechanical  defence,  for,  even  if  the  inner  table  be 
forced  inwards  by  a  blow,  the  dura  may  still  offer  a  successful 
resistance,  so  that  bony  debris,  effused  blood,  or  infective  material 
may  be  held  up  outside  it.  The  bony  cranium,  when  fractured  by 
a  blow,  may  either  remain  depressed  at  the  site  of  impact,  indenting 
the  dura,  or  it  may  recoil,  leaving  an  extra-dural  hsemorrhage 
from  one  of  the  meningeal  vessels  which  are  embedded  in  the  outer 
part  of  the  dural  coat.  The  dura  is  split,  here  and  there,  to  carry 
between  its  layers  various  important  venous  sinuses. 

The  dura  mater  is  the  chief  barrier  against  invasion  by  infective 
organisms  threatening  the  brain  from  without.  Even  when  a  gap 
has  been  made  in  it,  the  dura  can  still  make  a  final  effort  to  prevent 
infection  of  the  sub-dural  and  sub-arachnoid  space  by  the  formation 
around  the  gap,  within  a  few  hours,  of  defensive  entanglements  or 
adhesions  between  the  dura  and  the  pia-arachnoid. 

The  sub-dural  and  sub-arachnoid  spaces  form  an  almost  defence- 
less zone,  freely  bathed  by  the  cerebro- spinal  fluid.  If  this  fluid 
becomes  contaminated,  it  disseminates  infective  organisms  through- 
out the  brain  and  thence  downwards  into  the  spinal  meninges. 

Within  these  various  coverings  is  the  soft,  helpless  hrain- 
suhstance,  held  together  by  the  pia  mater,  a  delicate  network  of 
connective  tissue,  which  dips  into  all  the  cerebral  fissures  and  sulci, 
covers  the  convolutions,  furnishes  a  sheath  to  all  the  cranial 
nerves,  and  supports  in  its  meshes  the  arteries,  veins,  and  lym- 
phatics as  they  enter  or  leave  the  brain.  It  is  important  to  remember 
that  the  cerebral  arteries  and  veins,  and  especially  the  veins,  are 
very  loosely  supported  in  the  pia  mater,  so  that  haemorrhages, 
whether  venous  or  arterial,  on  the  surface  of  the  brain,  are  hable 
to  spread  widely  over  the  cortex.  Within  the  brain  substance,  on 
the  other  hand,  hsemorrhages  are  less  frequently  venous  than 
those  on  the  surface,  and  spread  somewhat  less  easily,  owing  to 
the  greater  resistance  offered  by  the  brain-tissue. 


ORGANIC   WAR-LESIONS  489 

The  cerebro-spinal  fluid,  which  fills  the  cerebral  ventricles  and 
bathes  the  sub-dural  and  sub-arachnoid  spaces,  together  with  the 
peri-vascular  and  peri-cellular  lymph-spaces,  is  collected,  here  and 
there,  into  larger  sub-arachnoid  cisterns  or  water-cushions,  notably 
in  the  mesial  inter-peduncular  space  and  laterally  in  the  ponto- 
cerebellar angles. 

Wounds  of  the  Head — These  may  be  produced  by  various  pro- 
jectiles, such  as  rifle,  revolver,  or  shrapnel  bullets,  shrapnel  fuses 
or  cases,  fragments  of  high- explosive  shells,  or  bombs.  Sword, 
bayonet,  and  rifle-butt  wounds  are  relatively  rare  in  modern 
warfare.  With  the  exception  of  a  very  small  proportion  (chiefly 
due  to  rifle  bullets),  all  the  wounds  thus  produced  are  septic,  i.e. 
infected  by  pyogenic  organisms. 

Cranial  wounds  may  be  divided  into  various  classes  : 

1.  Tangential  or  Glancing  Wounds,  in  which  the  bullet  or  metallic 
fragment  does  not  penetrate  the  cranial  cavity.  These  constitute 
the  great  majority  of  non-fatal  cases.  Out  of  a  series  of  118  per- 
sonally observed  cases  (exclusive  of  mere  scalp  wounds),  77,  i.e.  65 
per  cent.,  were  tangential,  18  (or  15  per  cent.)  were  through  and- 
through  wounds,  and  in  23  (or  20  per  cent.)  the  missile  remained 
within  the  cranium. 

Tangential  wounds  may  be  subdivided  into  : 

(a)  Scal'p  wounds,  which  are  generally,  but  not  always,  septic. 
If  uncomplicated,  scalp  wounds  generally  heal  under  simple 
treatment.  Every  scalp  wound,  however,  should  be  carefully 
examined,  lest  it  lead  down  to  a  fracture  of  the  subjacent 
cranium. 

(b)  Fractures  of  the  cranium  are  generally,  but  not  invariably, 
compound.  We  may  meet  with  fissured  fracture  of  both  tables, 
often  radiating  for  long  distances  from  the  site  of  the  blow,  and 
frequently  associated  with  extra-dural  haemorrhage.  The  extent 
of  a  fissured  fracture  is  best  determined  by  radiography.  Fissured 
fractures  often  extend  to  the  base  of  the  skull,  where  they 
may  implicate  various  foramina,  producing  cranial-nerve  palsies. 
Punctured  fracture,  in  which,  at  the  floor  of  a  scalp  wound,  there  is 
a  small  localised  aperture  in  the  cranium,  is  less  common  than  a 
fissured  fracture,  but  is  highly  dangerous  if  overlooked,  since  it  is 
frequently  associated  with  laceration  of  the  dura  and  with  infec- 
tion of  the  meninges  and  brain-substance.  Gutter  fracture  is  very 
common,  running  either  sagitally,  transversely,  or  obliquely,  and 


490  KERVOUS   DISEASES 

grooving  either  the  outer  table  alone,  exposing  the  diploe,  or,  more 
commonly,  affecting  both  tables  of  the  skull. 

Each  of  the  foregoing  fractures  is  Hable  to  be  associated  with 
defressed  fracture  of  the  inner  table,  always  more  extensive  than 
the  fracture  of  the  outer  table,  indenting  and  often  lacerating  the 
dura  mater. 

In  all  these  fractures  the  subjacent  brain-tissue  may  be  pulped 
by  the  impact,  or  there  may  be  a  superficial  cortical  haemorrhage 
from  laceration  of  the  thin- walled  surface-veins  or  from  penetration 
of  a  tough-walled  venous  sinus. 

In  every  compound  fracture  the  cardinal  point  to  determine 
is  whether  or  not  the  dura — ^the  great  barrier  against  intra-cranial 
infection — has  been  lacerated.  This  is  determined  by  careful  in- 
spection and  palpation  of  the  wound,  often  greatly  assisted  by  an 
X-ray  photograph.  A  probe  should  never  be  used  to  search  for  a 
gap  in  the  dura,  for  not  only  does  it  tend  to  make  a  false  track,  but 
it  may  push  infective  material  inwards  towards  deeper  structures. 
So  long  as  the  dura  is  untorn,  sub-dural  lesions  usually 
remain  free  from  infection  and  run  an  aseptic  course.  If,  how- 
ever, the  dura  be  lacerated,  the  brain-substance  is  now  in 
direct  continuity  with  the  septic  outer  world. 

2.  Penetrating  Wounds  of  the  Cranial  Cavity. — These  are 
wounds  in  which  bullets,  metallic  fragments,  bony  fragments, 
and  sometimes  portions  of  the  patient's  headgear  become  lodged 
within  the  dura  at  varying  depths  beneath  the  surface.  Some- 
times a  spray  of  bony  splinters  becomes  projected  deeply  into 
the  brain  substance  (see  Figs.  233  and  234),  whilst  the  bullet  itseK 
glances  off  or  merely  indents  the  cranium.  Sometimes  the  bullet, 
after  traversing  the  brain,  impinges  on  the  opposite  side  of  the 
skull,  where  it  either  produces  an  elevated  fracture  or  rebounds 
to  some  other  part  of  the  brain.  Metalhc  or  bony  fragments 
within  the  brain  are  often  multiple.  X-rays  are  of  the  greatest 
value  in  locahsing  them.  Here  again  a  probe  should  not  be  used 
for  their  detection.  Gentle  palpation  with  the  finger-tip  is  some- 
times permissible,  but  the  area  of  cortical  destruction  should  not 
be  increased  by  the  crude  method  of  introducing  the  finger  into 
the  brain- sub  stance. 

3.  Perforating,  or  Through-and-through,  Wounds  are  those  in 
which  the  missile  has  traversed  the  cranial  cavity,  entering 
through  one  and  coming  out  through  another,  generally  a  larger, 


ORGANIC   WAR-LESIONS  491 

opening.  The  edges  of  the  bony  apertures  are  usually  extensively 
comminuted,  and  from  them  fissured  fractures  radiate  in  various 
directions.  Haemorrhage  in  the  bullet-track  is  most  abundant  near 
the  point  of  entry,  and  tends  to  diminish  in  amount  in  the  deeper 
parts.  (See  Figs.  235  and  236.)  Many  of  these  cases  are  rapidly 
fatal  from  shock  to  the  vital  centres  in  the  brain-stem,  associated 
with  intra-cranial  haemorrhage.  Wounds  which  traverse  the 
cerebral  ventricles,  or  which  pass  through  the  brain-substance 
beneath  the  ventricles,   are   always  fatal.    A  few  through-and- 


Fict.  233.  Vi„.  234. 

Figs.  233  and  234. — Brain  sections  from  the  case  of  a  patient  who  was  admitted 
moribund  with  total  left-sided  hemiplegia  and  a  cranial  gap  in  the  right 
parietal  region.  An  area  of  softening  extends  through  the  centrum  ovale 
from  the  site  of  the  tangential  wound  to  jnst  outside  the  posterior  horn 
of  the  lateral  ventricle.  No  bullet  or  metallic  fragment  was  found 
within  the  brain.  The  haamorrhagic  area  was  most  marked  near  the  sur- 
■  face  (Fig.  233),  the  deeper  part  of  the  softened  area  being  free  from 
haemorrhage.  Numerous  bony  splinters  were  driven  deep  into  the  brain, 
being  most  numerous  immediately  outside  the  lateral  ventricle  (Fig.  234), 
which  was  not  penetrated. 

through  wounds,  however,  are  compatible  with  survival,  e.g. 
wounds  through  the  pre-frontal  lobes  or  through  the  upper  region 
of  the  cerebral  hemisphere  above  the  level  of  the  ventricles. 

4.  Large  Cranial  Gaps,  with.  Extensive  Comminution,  may  be 
produced  either  by  glancing  blows  from  a  large  missile,  or  as 
exit-openings  of  through-and-through  wounds.  Most  of  them  are 
fatal.  A  few  patients  survive,  if  adequate  drainage  can  be  pro- 
vided and  general  intra-cranial  infection  prevented — a  rare  and 
lucky  occurrence. 


492 


NERVOUS   DISEASES 


Morbid  Anatomy  of  Brain  Wounds. — Except  in  the  case  of 
injuries  at  close  range,  or  by  large  fragments  of  shell,  as  a  result 
of  which  portions  of  the  skull  and  brain  may  be  blown  away,  sutures 
torn  apart  and  the  cranial  base  burst  open,  the  amount  of  actual 
destruction  of  nerve-cells  and  nerve-fibres  produced  directly,  by 
the  bullet  itself,  is  relatively  small.  Most  of  the  structural 
damage  which  results  is  caused  by  hsemorrhage,  septic  infection, 
or  other  secondary  event.      Moreover,  the  severity  of  a  cerebral 


Fig.  235. 


Fig.  236. 


Figs.  235  and  236. — Perforating  wound  of  brain.  The  point  of  entry  is  at  the 
posterior  end  of  the  left  occipital  lobe,  one  inch  from  the  middle  line.  The 
bullet-track  crosses  the  middle  line  above  the  level  of  the  corpus  callosum, 
and  emerges  through  the  posterior  end  of  the  second  frontal  gyrus  on  the 
right  side. 

The  heemorrhage  in  the  bullet-track  is  most  abundant  in  the  left  occi- 
pital lobe,  diminishing  in  amount  as  the  track  traverses  the  right  cerebral 
hemisphere.  The  anterior  end  of  the  track  consists  of  disintegrated  brain- 
tissue,  free  from  hemorrhage,  except  immediately  around  the  aperture  of 
exit,  where  there  are  a  few  petechial  points  in  the  cortex  and  sub-cortex. 

lesion  is  not  necessarily  proportional  to  that  of  the  cranial  injury. 
War  injuries  are  usually  in  young  and  healthy  brains,  free  from 
vascular  or  degenerative  disease.  Rarely  is  a  cortical  centre  com- 
pletely destroyed,  so  that  in  almost  every  case  of  survival,  a  cer- 
tain amount  of  recovery  may  be  expected.  Cerebral  concussion 
at  the  time  of  the  injury  is  common,  with  its  frequent,  feeble 
pulse,  low  blood-pressure,  and  shallow,  irregular  respiration,  fol- 
lowed, if  the  patient  survives,  by  a  stage  of  reaction,  with  headache, 


ORGANIC   WAR-LESIONS  493 

flushed  face,  high  blood-pressure,  and  powerfully-beating  heart 
(see  p.  62).  Concussion  varies  in  degree  in  different  cases,  and  is 
not  always  proportional  to  the  apparent  severity  of  the  Vjlow. 
Thus  in  one  case  a  comparatively  slight  head-injury,  without 
fracture  of  the  skull,  may  produce  severe  concussion  or  other  intra- 
cranial Eymptoms,  whereas  another  patient  may  sustain  a  severe 
cranial  lesion,  or  even  a  perforating  wound,  and  yet  concussion 
symptoms  may  be  shght  or  transient.  Cerebral  compression,  from 
intra-cranial  haemorrhage,  produces  a  characteristic  and  easily- 
recognised  syndrome  (see  p.  65),  which  is  often  preceded  by  a 
stage  of  cerebral  irritation,  during  which  the  patient  lies  curled  up 
in  bed,  with  all  his  limbs  flexed,  burying  his  head  under  the  bed- 
clothes owing  to  photophobia,  and  resenting  any  examination, 
noise,  or  conversation.  Meantime  he  suffers  from  violent  headache, 
whilst  the  temperature  is  raised  to  101°  or  102°  F. 

Meningeal  adhesions  usually  develop  within  a  few  hours  around 
any  wound  in  the  dura  mater.  These  adhesions  are  nature's  effort 
to  shut  off  the  infected  area  from  the  cerebro -spinal  lymph  system 
and  thus  to  prevent  a  diffused  meningeal  infection.  Meningeal 
adhesions  of  this  sort  constitute  a  barrier  which  should  be  treated 
with  the  greatest  respect,  and  should  not  be  broken  down  by  the 
svirgeon. 

Structural  damage  of  brain  tissue  is  mainly  due  to  the  following 
secondary  processes  : 

1.  Contusion  or  laceration  by  hcemorrhage,  which  may  be 
superficial  or  deep.  A  superficial  haemorrhage,  sub-dural  or  sub- 
pial,  is  not  necessarily  arterial.  It  is  often  due  to  tearing  of  cortical 
veins  by  a  depressed  fragment  of  bone,  or  to  rupture  of  thin-walled 
surface-veins  near  their  point  of  entry  into  the  rigid  superior 
longitudinal  sinus.  Superficial  haemorrhage,  whether  arterial  or 
venous,  produces  signs  of  cortical  lesion,  varying  with  the  particular 
region  affected.  Thus  in  the  motor  cortex  we  have  localised 
paralysis  with  muscular  rigidity  and  sometimes  Jacksonian  fits ; 
in  the  sensory  cortex,  anaesthesia  of  cortical  type  ;  in  the  visual 
cortex,  impairment  of  vision,  sometimes  preceded  by  subjective 
luminous  sensations,  and  so  on.  There  are  also  various  "  silent 
areas "  of  the  brain  which  may  be  severely  damaged  without 
producing  any  obvious  focal  signs  whatever. 

Deeper-seated  haemorrhage  within  a  bullet-track  is  generally 
more  marked  near  the  surface  of  the  brain.     It  may  sometimes 


494 


NERVOUS   DISEASES 


extend  througliout  tlie  track  of  disintegrated  brain-substance,  but 
often  the  deepest  part  of  the  wound  is  practically  free  from 
bsemorrliage. 

Severe  contusions  of  the  brain- sub  stance  may  occur  from  a 
bullet-wound  of  the  head  apart  from  traversing  the  cranial  cavity 
or  laceration  of  the  dura  mater,  as  in  the  case  shov/n  in  Fig.  237. 

In  this  case  the  bullet  entered  the  head  in  the  mid-frontal  region, 
half  an  inch  above  the  nasion.     It  then  traversed  the  right  orbit, 


Fig.  237. — Contusion  of  right  temporal  lobe,  wiih  fracture  of  cranial 
base,  from  extra-dural  bullet-wouud. 


producing  paralysis  of  the  ocular  muscles,  and  emerged  below  the  right 
mastoid  process,  fracturing  the  lower  jaw  and  paralysing  the  right 
facial  nerve  en  route. 

At  the  autopsy  the  dura  mater  was  found  intact,  but  there  was  a 
fracture  of  the  cranial  base,  implicating  the  cribriform  plate  and  floor 
of  the  right  middle  fossa  of  the  skull.  The  anterior  part  of  the  right 
temporal  lobe  was  severely  contused,  and  also  slightly  the  orbital 
surface  of  the  right  frontal  lobe. 

In  rare  cases  a  second  cerebral  haemorrhage  may  occur  inde- 
pendently of  the  bullet  wound,  thereby  compUcating  the  diagnosis, 
as  in  the  following  case  (Figs.  238  and  239)  : — 

A  patient  who  had  sustained  a  perforating  trans-frontal  wound, 
entering,  through  one  temporal  fossa  and  emerging  at  the  other,  was 


ORGANIC   WAR-LESIONS 


495 


admitted    witli   complete   left-sided   flaccid    heniijjlegia.    The   trans- 
frontal  wound  was  insufHcient  to  accoimt  for  his  symptoms.     These 


Fig.  238. — Transfrontal  wound.     Entry  through  right  Sylvian  point. 
Exit  through  left  frontal  lobe,  at  posterior  end  of  F3  gyrus. 

were  explained,  however,  at  the  autopsy,  which  showed  an  independent 
haemorrhage,  the  size  of  a  walnut,  above  and  behind  the  right  internal 


Fig.  239. — -HEemorrhage  in  right  centrum  ovale,  from  the  case 
of  transfrontal  wound  shown  in  Fig.  238. 

capsule,  at  a  considerable  distance  from  the  bullet  track  through  the 
frontal  lobes. 


496  NEEVOUS   DISEASES 

2.  Acute  cerebral  softening  or  necrosis  of  brain-tissue  occurs  along 
the  track  of  a  bullet  wound.  It  also  occurs  tbrougbout  tbe  area 
of  brain  destruction  produced  by  the  sudden  impact  of  a  projectile, 
whether  the  superjacent  cranium  and  dura  be  lacerated  or  not. 
The  superficial  part  of  the  softened  area  then  becomes  infiltrated, 
to  a  varying  extent,  by  effused  blood,  forming  a  hsemorrhagic 
softening,  whilst  the  rest  of  it,  especially  at  the  deepest  part  from 
the  surface,  may  remain  as  a  pale  area  of  simple  disintegration, 


Fig.  240. — Transverse  wound  of  frontal  bone,  causing  deep-spread  abscess 
of  right  frontal  lobe,  with  a  second  commencing  abscess  at  tip  of  left 
prefrontal  region. 

free  from  haemorrhage.     Such  a  softened  area,  if  infective  organisms 
gain  access  to  it,  readily  develops  into  an  abscess. 

3.  CEdema  of  the  brain-tissue,  around  the  contused  or  lacerated 
area,  is  a  common  occurrence.  It  is  due  to  local  obstruction  of 
the  venous  circulation.  This  oedema  throws  out  of  action,  for  a 
time,  a  wider  area  of  brain-tissue,  with  a  corresponding  increase 
in  the  extent  of  the  focal  signs  and  symptoms.  Fortunately  it 
tends  to  subside  gradually,  and  with  it  the  brain  symptoms  corre- 
spondingly recede. 

4.  Abscess  (or  suppurative  encephahtis)  may  form  around 
the  infected  track  within  the  brain.  Unless  successfully  evacuated 
and  drained  externally,  the  suppurative  process  tends  to  spread 


ORGANIC   WAR-LESIONS 


497 


inwards,  and  ultimately,  after  weeks  or  even  months  (even 
after  the  original  wound  may  have  healed  on  the  surface), 
may  reach  one  of  the  ventricles  of  the  brain  (see  Fig.  240).  Death 
is  then  inevitable  within  a  few  days,  from  infection  of  the  cerebro- 
spinal fluid.  There  is  sometimes  a  premonitory  stage  of  shght 
pyrexia  with  reappearance  of  traces  of  the  former  focal  signs.  The 
infection  passes  outwards  from  the  ventricles,  through  the  great 
transverse  fissure,  to  the  base  of  the  brain,  and  thence  all  over  the 
meninges,  from  base  to  vertex.  Retained  foreign  bodies,  whether 
fragments  of  bone  or  bullets,  which  have  carried  infection  inwards, 
are  frequent  causes  of  brain  abscess,  but 
abscess  may  also  occur  even  when  no  foreign 
body  is  present.  Suppuration  is  specially 
common  within  or  near  a  cerebral  hernia. 

5.  Diffuse  purulent  meningitis  is  the  cause 
of  death  in  three-fourths  of  the  fatal  cases 
(apart  from  immediate  fataKties  on  the  field). 
It  is  generally  more  severe  at  the  base  of  the 
brain  than  on  the  convexity.  Sometimes  the 
meningeal  infection  spreads  directly  from  the 
neighbourhood  of  the  wound  in  the  dura, 
before  there  has  been  time  for  defensive 
adhesions  to  fence  off  the  sub -arachnoid 
space.  In  other  cases  infection  of  the 
cerebro-spinal  fluid  and  meninges  occurs  from 
subsequent  operative  procedures,  which  break 
down  protective  adhesions,  e.g.  during  an 
attempt  to  reach  a  foreign  body  within.  In 
other  cases,  again,  meningitis  is  secondary 
to  infection  of  the  cerebral  ventricles,  and  it  is  in  this  way  that 
a  large  proportion  of  cerebral  abscesses  cause  death. 

Hernia  cerebri  is  a  condition  in  which  a  bulging  mass  of 
brain  tissue  is  prolapsed  through  a  cranial  opening  (see  Figs.  241 
and  242).  The  contents  of  the  hernial  swelling  are  cerebro- 
spinal fluid  and  brain-tissue,  in  varying  proportions  in  different 
hernise.  The  swelling  usually  pulsates,  synchronously  with  the 
heart-beats. 

Hernia  cerebri  is  caused  by  increased  intra-cranial  pressure, 
whether  from  meningitic  changes  following  a  brain-wound  or  from 
the  continued  growth  of  an  inoperable  intra-cranial  growth.     Some- 

2  1 


Fia.  2-il.— Bullet-wound 
of  right  frontal  lobe. 
The  only  abnormal 
sign,  on  examination 
of  the  nervous  system, 
was  absence  of  the 
left  abdominal  reflex. 
Together  with  this 
there  was  incontin- 
ence of  urine.  There 
was  no  paralysis,  sen- 
sory or  motor,  and  the 
mental  functions  were 
unimpaired. 


498 


NERVOUS   DISEASES 


times  a  hernia  cerebri  occurs  after  a  decompressive  craniectomy 
for  the  reUef  of  intra-cranial  pressure,  e.g.  from  brain  tumour.  The 
mere  presence  of  a  gap  in  the  cranium  does  not  cause  a  healthy  brain 
to  prolapse  through  the  gap  (see  Eig.  243).  Hernia  cerebri  following 
a  brain  wound  is  therefore  always  a  sign  of  sepsis.  In  cases  that 
are  getting  worse,  from  increasing  intra-cranial  pressure,  the 
herniated  tissues  often  become  oedematous  owing  to  strangulation 
of  the  neck  of  the  hernia  by  the  rigid  dura  and  bone.  Pulsation 
then  diminishes  and  disappears,  and  the  hernia  forms  a  fungus- 
like mushroom- shaped  mass,  which  may  subsequently  slough  away. 


Fig.  242. — Hernia  cerebri  of  right  pre-  and  post-central  region, 
associated  witli  progressive  left  hemiplegia. 

It  is  remarkable  how  large  an  area  of  cerebral  tissue  may  be  in 
some  cases  prolapsed  into  a  hernia  without  producing  paralysis 
or  other  symptoms.  Subsidence  of  a  hernia  is  a  favourable  sign, 
and  indicates  that  the  intra-cranial  pressure  is  subsiding. 

Transient  opic  neuritis  develops  with  a  large  proportion  of  the 
more  severe  brain-wounds.  It  does  not  necessarily  foreshadow  a 
cerebral  abscess  or  a  septic  meningitis.  It  comes  on  within  a  day 
or  two  of  the  original  injury,  and  is  probably  caused  by  serous 
meningitis  or  meningo- encephalitis,  secondary  to  the  local  haemor- 
rhage or  other  lesion. 


ORGANIC   WAR-LESIONS 


499 


Focal  Signs  of  Brain  Injuries 
(1)  Lesions  of  the  cortical  motor  areas  of  the  pre-central  region 

and  of  the  adjacent  posterior  end  of  the  second  frontal  gyrus 
(Fig.  3,  p.  5)  are  the  easiest  of  all  to  recognise,  since  destmction 
of  these  centres  produces  monoplegia,  facial,  brachial,  or  crural, 
as  the  case  may  be — or,  in  more  extensive  lesions,  hemiplegia  of 
the  contra-lateral  side.  Superficial  lesions  such  as  sub-pial 
haemorrhage,  or  localised  meningitis,  or  a  depressed  fracture 
pressing  on   the    cortex,  may  also    cause   Jacksonian  fits,    which 


Fkj.  243. —Bullet-wound  of  right  frontal  lobe,  without  hernia 
cerebri.  No  mental  affection.  No  incontinence  of  urine. 
No  abnormalitj^  of  cranial  nerves,  nor  of  sensory  or  motor 
functions,  save  for  absence  of  both  abdominal  reflexes. 

commence  in  the  corresponding  muscular  group.  These  Jack- 
sonian fits  are  usually  followed  by  a  temporary  increase  of 
paralysis  in  the  previously  convulsed  limb.  A  localised  fit  of  this 
sort  may  either  remain  limited  to  one  limb,  or  segment  of  a  limb, 
or  it  may  spread  so  as  to  affect  the  muscles  of  the  whole  of  that 
side  of  the  body.  It  may  then  cross  the  middle  line,  becoming 
bilateral,  with  unconsciousness  and  tongue-biting.  Even  without 
Jacksonian  fits,  it  is  not  uncommon  to  have  marked  tonic  rigidity 
of  the  paralysed  or  paretic  limb.  This  is  always  suggestive  of  a 
superficial  lesion  such  as  a  sub-dural  haemorrhage. 

Lesions  confined  to  the  upper  end  of  the  pre-central  gyrus 
(Fig.  244,  p.  500)  produce  crural  monoplegia,  those  at  the  lower 
end  cause  facial  (Fig.  245)  or  f  acio-lingual  monoplegia  (Figs.  246  and 
247),  whilst  lesions  half-way  down  the  pre-central  gyrus  cause 


500 


NERVOUS   DISEASES 


brachial  monoplegia.     A  purely  cortical  lesion,  in  order  to  produce  a 

complete  hemiplegia,  must  extend 
from  the  upper  to  the  lower  end  of 
the  pre-central  gyrus.  If,  however, 
the  lesion  is  sub -cortical,  the  more 
deeply  it  penetrates  through  the 
centrum  ovale  towards  the  internal 
capsule,  the  more  completely  are 
the  converging  fibres  of  the  pyra- 
midal tract  involved,  so  that  quite 
a  small  lesion,  if  deeply  situated 
in  the  white  matter  of  the  internal 
capsule,  may  produce  complete 
hemiplegia.  In  other  words,  the 
more  superficial  the  lesion,  the 
greater    the    tendency   to    mono- 

FiG.  244.— Bullet-wound  immediately  plegia  ;  the  deeper  the  lesion,  the 
to  left  side  of  middle  line,  exactly  ^^^^  ^-j^^^  ^^^^  ^^  ^^  ^^^  j^g^^-. 
over   upper   end    or    pre-central  _  ■' 

gyrus.    Horse-shoe  flap,  crossing  plegia,     often     accompanied     by 
"S.  'Sem1dSL33!  temianaesthesia  and  even  by  hemi- 

Kolandic  fissure  are  also  marked    anopia  (see  pp.  9  and  10). 

on  the  scalp.  Tangential  wounds  of  the  vertex 

often    cause   a  bilateral   lesion   of  the  upper  ends  of  both  pre- 


FiG.  245.— Shell  wound  at  right  Rolandic  fissure,  causing  left 
facial  monoplegia. 

central    gyri,    producing    bilateral    monoplegia    of    both    legs- 
crural  diplegia. 


ORGANIC   WAR-LESIONS 


501 


Left-sided  lesions  of  the  pre-central  region,  when  they  imphcate 
the  motor  speech-centre  in  Broca's  convolution,  or  the  sub-cortical 


Fig.  246. — Bullet- wound  of  head,  producing  pre-  and  post-Kolandic 
lesion,  with  left-sided  facio-liDgual  monoplegia,  also  loss 
of.J  joint-sense  [in  left  hand,  with  astereognosis,  but  without 
motor  weakness  of  limbs. 


Figs.  247  and  247a.  — Left-sided  facio-lingual  monoplegia  from  the  cortical  wound 
shown  in  Fig.  246;  Fig.  247  shows  the  condition  at  rest,  Fig.  247a  the 
appearances  on  protruding  the  tongue. 


502  NERVOUS   DISEASES 

fibres  connecting  it  witli  the  other  speech-centres,  produce  motor 
aphasia,  in  addition  to  monoplegia  or  hemiplegia,  as  in  the  fol- 
lowing case  : — 

The  patient  was  admitted  to  hospital  unable  to  furnish  any  account 
of  his  previous  history.  He  had  a  small  bullet  hole  in  the  scalp,  two 
inches  to  the  left  of  the  middle  line  and  one  inch  in  front  of  the  middle 
of  the  Rolandic  fissure.  The  patient  was  unable  to  utter  any  sounds, 
not  even  "yes"  or  "no."  He  was  able,  however,  to  understand  and 
execute  with  ease  both  written  and  verbal  requests.  On  trying  to 
write  with  his  left  hand,  he  made  such  gross  spelling  mistakes  as  to 
be  unintelligible — e.g.  for  "doctor"  he  wrote  "  dorocks."  There  was 
marked  right-sided  facio-brachial  monoplegia,  the  upper  limb  being 
totally  paralysed  and  flaccid  at  all  joints.  The  right  lower  limb  was 
only  slightly  feeble  and  dragged  a  little  in  walking.  The  right 
supinator-] erk  was  absent,  the  left  present ;  the  knee-jerks  and  ankle- 
jerks  were  normal  and  equal ;  the  plantar  reflexes  were  both  flexor  in 
type  ;  the  left  abdominal  reflex  was  absent,  the  right  present. 

On  exploring  the  bullet  wound,  which  was  apparently  about  four 
or  five  days  old,  a  few  fragments  of  metal  were  found  in  the  outer 
table,  but  there  was  no  depression.  A  trephine-disc  of  bone  was  re- 
moved, and  on  incising  the  uninjured  dura,  immediately  subjacent,  a 
mass  of  blood-clot  was  at  once  extruded  from  the  sub-cortical  brain- 
tissue  at  that  point.  Next  day,  at  the  first  dressing,  a  further  amount 
of  blood-clot  also  came  away. 

Ten  days  after  operation,  although  still  unable  to  speak,  the  patient 
could  write  simple  words  to  dictation,  and  could  also  copy  accurately  and 
add  up  columns  of  figures,  using  his  left  hand.  The  right  upper  limb 
was  beginning  to  regain  some  power.  A  month  after  his  operation 
he  began  to  recover  motor  speech,  the  first  word  he  said  being 
"  Thursday."  Next  day  he  could  form  short  sentences,  and  within  a 
week  was  able  to  speak  in  normal  fashion,  although  with  great  delibera- 
tion.    The  monoplegia  of  the  face  and  arm  completely  cleared  up. 

(2)  Lesions  of  the  post-central  gyrus  form  a  most  interesting 
group.  Their  symptoms  are  essentially  sensory.  If  the  lesion 
implicates  the  uppermost  or  mesial  end  of  the  post-central  gyrus  the 
symptoms  are  confined  to  the  contra-lateral  toes  and  ankle.  Pro- 
ceeding along  this  gyrus  from  above  downwards,  the  cortical 
sensory  centres  correspond  in  level  with  the  pre-Rolandic  motoT 
centres  for  the  knee,  hip,  shoulder,  elbow,  hand,  &c.,  on  the 
other  side  of  the  central  fissure. 

The  clinical  signs  of  a  post-central  lesion  consist  in  the  presence 
of  one  or  more  varieties  of  sensory  loss  in  the  contra-lateral  limb. 
In  some  cases  we  observe  a  degree  of  blunting  of  cutaneous 
sensation  to  light  touches,  most  marked  at  the  periphery  of  the 


ORGANIC   WAR-LESIONS 


503 


limb  and  fading  as  we  ascend  towards  its  proximal  end.  One 
of  the  chief  characteristics  of  this  cortical  type  of  cutaneous 
deficiency  is  its  untrustworthiness  of  response  and  its  excessive 
tendency  to  fatigue,  so  that  responses  to  touches  tend  to  disappear. 
The  compass-test  in  these  cases  shows  definite  widening  of  the 
distance  at  which  a  pair  of  blunt  compass-points  are  recognised 
as  separate.  Still  more  striking  is  the  loss  of  joint-sense  in  the 
affected  limb  or  segment  of  a  limb,  so  that,  with  the  eyes  shut, 
when  the  patient's  joint  is 
passively  moved  from  the 
flexed  to  the  extended  posi- 
tion, or  vice  versa,  he  fails  to 
recognise  its  posture.  This 
loss  of  joint-sense  often  pro- 
duces marked  clumsiness  of  the 
affected  hand  or  foot,  which 
is  aggravated  if  the  patient 
closes  his  eyes.  Astereognosis 
is  another  characteristic  feat- 
ure of  post-central  lesions, 
and  is  generally,  but  not 
always,  proportional  to  the 
loss  of  joint-sense.  Stereo- 
gnosis  is  tested  by  closing  the 
patient's  eyes  and  then  placing 
some  familiar  object,  e.g.  a 
coin,  a  key,  a  pair  of  scissors, 
or  a  watch,  in  his  hand.  In 
the  case  of  the  foot,  we  may 


Fig.  248. — Left-sided  post  -  Rolandic 
wound  of  braiu,  producing  profound 
loss  of  joint-sense  in  right  fingers 
and  hand  with  astereognosis  of  right 
hand  and  inability  to  hold  objects  in 
it  with  eyes  shut._ 


use  for  the  same  purpose  a  brush,  a  sponge,  a  chain,  or  one's  own 
finger,  as  the  test  object,  all  of  these  being  easily  recognised  by 
a  normal  foot. 

(3)  Combined  pre-  and  post-central  lesions  are  commoner  than 
pure  lesions  limited  to  the  pre-central  or  post-central  gyms  alone. 
The  symptoms  of  a  combined  lesion,  which  may  be  unilateral  or 
bilateral,  depend  upon  the  level  at  which  the  Rolandic  fissure  is 
crossed,  and  also  on  the  proportional  involvement  of  the  pre-central 
or  motor  and  of  the  post- central  or  sensory  cortex.  Bilateral 
lesions  are  usually  the  result  of  a  glancing  wound  of  the  vertex 
catching  the  upper  ends  of  both  Rolandic  regions  and  producing 


504 


NERVOUS    DISEASES 


a  diplegia,  generally  asymmetrical  and  with  its  most  profound 
symptoms  in  the  lower  limbs.  These  lesions  are  best  understood 
by  studying  a  few  illustrative  cases  : — 

Fig.  249  shows  a  patient  in  whom  there  was  a  punctured  depressed 
fracture,  two  inches  to  the  right  of  the  middle  line  and  exactly  over 
the  Rolandic  fissure.  There  was  an  irregular  hole  in  the  dura,  from 
which  were  extracted  by  Lt.-Col.  Legg,  at  an  operation  six  days  after 
the  injury,  two  fragments  of  inner  table,  one  inside,  the  other  outside. 


Fig.  249. — Left  facial  I'emiplegia  from  cortical  pre-  and  post-Kolandic 
lesion.  The  left  arm  was  also  paralysed,  with  astereognosis  and 
loss  of  joint-sense,  &c. 

the  dura  mater,  together  with  intra-  and  extra-dural  blood-clot.  From 
the  outset  the  patient  had  well-marked  left-sided  facial  hemiplegia 
(Fig.  249),  also  complete  paralysis  of  the  left  upper  limb,  accompanied 
by  some  flexor  rigidity  of  the  shoulder  and  elbow.  The  left  lower  limb 
was  only  slightly  weaker  than  the  right.  To  light  cotton-wool  touches 
there  was  no  loss  of  sensation,  although  they  felt  "  different  "  in  the 
left  hand  and  forearm.  Pin-pricks  were  felt  equally  on  both  sides. 
The  compass  test  yielded  3  cm.  in  the  right  hand  and  10  cm.  in  the 
left ;  in  the  right  foot  2  cm.,  in  the  left  11  cm.  Jomt-sense  was  lost  at 
all  joints  of  the  left  upper  limb  and  at  the  left  toes,  ankle,  and  knee. 
There  was  astereognosis  of  the  left  hand  (with  coin,  chain,  and  key) 
and  of  the  left  foot  (with  chain,  brush,  and  sponge).  The  left  plantar 
reflex  was  absent,  the  right  was  of  the  normal  flexor  type.     The  left 


ORGANIC   WAR-LESIONS 


505 


abdominal  reflex  was  absent,  the  right  was  present.  The  left  biceps- 
jerk  was  brisker  than  the  right ;  the  knee-jerks  and  ankle-jerks  were 
normal  and  equal  on  the  two  sides. 

Two  weeks  after  the  original  wound,  the  facio-brachial  monoplegia 
still  persisted,  whereas  the  weakness  of  the  lower  limb  had  disappeared. 
Ankle  clonus,  however,  was  now  elicited  on  the  left  side.  The  loss  of 
joint  sense,  widened  compass  test,  and  astereognosis  still  persisted  in 
the  left  upper  and  lower  limbs. 

Fig.  250  is  another  example  of  a  combined  pre-  and  post-central 
lesion  in  a  young  Australian  officer.  There  was  a  gutter  fracture  of 
the  vertex,  starting  just  to  the  left  of  the  middle  line  in  front  of  the 
central  fissure,  extending  obliquely  backwards  and  to  the  right,  and 
crossing  the  upper  end  of  the  right  Rolandic  fissure.  On  recovering 
consciousness   a  few  minutes  after  the  injury,    his  left  arm  and  leg 


Fig.  250. — Vertical  wound,  crossing  middle  line. 
Pre-  and  post-central. 

were  powerless  for  aboutjhalf  an  hour.  The  weakness  of  the  arm 
then  cleared  up,  but  the  left  lower  limb  remained  weak,  especially 
at  the  toes  and  ankle,  which  were  completely  paralysed.  There  was 
also  some  motor  weakness  of  the  right  foot,  which  persisted  for  a  week 
or  two.  Four  days  after  being  wounded  he  had  a  left-sided  Jacksonian 
fit,  beginning  in  the  muscles  around  the  left  shoulder  and  spreading 
to  the  left  face  and  left  lower  limb.  When  examined  six  days  after 
the  injury,  his  symptoms  corresponded  accm'ately  with  the  cortical 
lesions.  Thus  the  movements  of  the  toes  and  ankles  were  impaired 
on  both  sides,  the  paralysis  being  partial  in  the  right  foot  and  complete 
in  the  left.  The  knee  and  hip  were  weak  on  the  left  side  only.  The 
upper  limbs  and  face  were  normal  and  symmetrical. 

The  foregoing  phenomena  were  obviously  due  to  lesion  of  the  upper 


506 


NERVOUS   DISEASES 


ends  of  the  pre-central  convolutions,  more  marked  on  the  right  side 
of  the  cerebrum.  The  sensory  phenomena,  from  lesion  of  the  right 
post-central  gyrus,  were  highly  characteristic.  Thus  the  compass  test 
yielded  10  cm.  on  the  left  foot  as  compared  with  5  cm.  on  the  right ; 
joint-sense  was  lost  in  the  left  toes  and  ankle,  and  there  was  astereo- 
gnosis  of  the  left  foot  only,  tested  with  brush  and  chain.  As  the  left 
lower  limb  regained  its  motor  power,  it  showed  marked  ataxia  with  the 
heel-knee  test,  and  the  patient  had  great  difficulty  in  walking,  more 
from  unsteadiness  than  from  actual  weakness  of  the  left  leg. 

(4)  Lesions  of  the  occipital  lobe  may  be  unilateral  or  bilateral. 
Here  the  most  important  point  to  determine  is  whether  the  half- 
vision  centre,  which  is  situated  mainly  on  the  mesial  aspect  of  the 


Fig.  251. — Radiogram  of  shrapnel  bullet  in  left  occipital  lobe. 
Seen  from  the  front,  the  bullet  appears  at  the  back  of  the 
left  orbit. 

hemisphere  (see  Figs.  3  and  4),  has  been  damaged.  Unilateral 
destruction  of  the  half-vision  centre  of  one  occipital  lobe  causes 
homonymous  hemianopia  of  the  contra-lateral  halves  of  both  visual 
fields.  If  the  lesion  be  limited  to  the  cortex  above  the  calcarine 
fissure,  only  the  lower  quadrant  of  each  haK-field  is  affected — a 
lower  quadrantic  hemianopia.  If  the  lesion  be  confined  to  the 
cortex  below  the  calcarine  fissure — a  much  rarer  occurrence — an 
upper  quadrantic  hemianopia  results.  Bilateral  occipital  lesions 
cause  total  blindness. 

In  quite  a  number  of  cases  the  haemorrhage,  oedema,  &c.,  around 
the  original  brain-wound  become  partially  or  wholly  absorbed, 
so  that  the  residual  permanent  lesion,  with  its  corresponding  visual 


ORGANIC   WAR-LESIONS 


507 


impairment,  is  much  less  than  would  be  expected  if  we  examine 
the  patient  within  a  few  hours  or  days  after  his  injury.  Thus  Fig. 
251  is  a  radiogram  of  a  patient  who  had  a  shrapnel  bullet  entering 
through  the  right  temporo-parietal  region  and  lodging  in  the  left 
occipital  lobe.  The  bullet-track  thus  traversed  both  occipital 
lobes.  A.S  a  result  he  was  at  first  completely  bhnd.  After  three 
weeks,  however,  he  gradually  regained  perception  of  light  in  the 
left  halves  of  both  visual  fields,  showing  that  the  half -vision  centre 
in  the  right  occipital  lobe  had  not  been  completely  destroyed. 

A  typical  example  of  a  clearing-up  lesion  of  one  occipital  lobe 
may  here  be  mentioned.     It  will  be  noted  that  the  lesion  was  on 


Fig.  252. — Lesion  of  left,  upper  occipital  region. 

the  outer  aspect  of  the  lobe,  so  that  the  calcarine  region  was  not 
directly  implicated. 

Fig.  252  is  that  of  a  patient  who  received  a  small  glancing  wound  in 
the  upper  occipital  region,  1 J  inches  to  the  left  of  the  middle  line,  at 
a  level  2 J  inches  above  the  external  occipital  protuberance.  The 
scalp  wound  was  incised  horizontally  and  explored,  but  no  fracture 
was  present  in  the  outer  table.  Immediately  after  being  hit,  this 
patient  noticed  that  he  was  unable  to  see  objects  on  his  right  side,  so 
that  he  stumbled  against  people  and  things,  as  he  walked  back  to  the 
dressing-station.  This  hemianopia  lasted  a  week  or  more.  When 
examined  more  carefully,  twelve  days  after  the  injury,  there  was  no 
limitation  in  the  size  of  either  visual  field,  but  the  visual  acuity  in  the 
right  halves  of  both  fields  was  markedly  diminished.  There  was  no 
other  sio;n  of  focal  intra-cranial  lesion. 


508 


NERVOUS   DISEASES 


Another  instance  of  a  similar  lesion  was  that  of  an  officer  who  sus- 
tained a  glancing  wound,  by  the  fuse  of  a  shell,  in  the  right  upper 
occipital  region  (Fig.  253),  causing  a  cranial  gap  whose  centre  was' one 
inch  to  the  right  of  the  middle  line  and  3f  inches  above  the  level  of  the 
external  occipital  protuberance.  The  wound  was  laid  open  by  a  crucial 
incision,  and  there  was  left  a  small  gap,  through  which  for  several 
weeks  a  cerebral  hernia  protruded  and  then  finally  subsided.  Five 
days  after  his  original  wound  there  was  marked  diminution  of  visual 
acuity  in  the  left  lower  quadrant  of  both  visual  fields.  The  fields 
themselves  were  not  contracted  on  either  side.     The  patient  also  had 


Fig.  253. — Lesion  of  right  upper  occipital  region. 

well-marked  astereognosis  and  loss  of  joint-sense  in  the  left  toes  and 
ankle,  with  widening  of  the  compass  test  in  the  left  foot  to  10  cm., 
as  compared  with  4  cm.  in  the  right.  These  sensory  symptoms  pointed 
to  implication  of  the  upper  end  of  the  post-central  gyrus,  either  from, 
oedema  or  from  forward  extension  of  the  occipital  haemorrhage.  The 
leg  symptoms  rapidly  cleared  up,  but  for  a  time  the  patient  still  felt 
momentarily  confused  when  he  looked  hurriedly  towards  objects  seen 
in  his  left  lower  fields. 

(5)  Lesions  of  the  frontal  lobes,  unless  they  implicate  the  posterior 
part  of  the  lobe  adjacent  to  the  pre-central  motor  areas,  are  often 
conspicuous  for  the  scarcity  or  absence  of  focal  signs.  Sometimes 
frontal  lesions  are  associated  with  an  alteration  in  the  patient's  char- 
acter, the  change,  unfortunately,  being  usually  for  the  worse.     Thus 


ORGANIC   WAR-LESIONS  509 

one  patient  sustained  a  through-and-througli  transfrontal  wound, the 
bullet  entering  through  one  temporal  fossa  and  passing  out  through 
the  other  ;  the  only  focal  signs  were  a  transient  monoplegia  of  the 
right  face,  and  loss  of  the  right  abdominal  reflex,  both  of  which 
signs  cleared  up  completely  within  a  couple  of  weeks.  Shortly 
afterwards,  during  convalescence,  he  ran  away  with  a  friend's 
wife.  Uncharitable  observers  may  perhaps  be  sceptical  as  to  the 
traumatic  origin  of  this  incident.  (There  was  no  history  of  a  frontal 
lesion  in  the  lady.)  Another  officer,  suffering  from  an  abscess  in 
the  left  frontal  lobe,  following  a  perforating  bullet-wound,  stole 
some  money  from  the  clothes  of  another  patient  who  died  in  the 
same  ward,  alleging  as  a  pretext,  when  charged  with  the  offence, 
that  the  dead  man  had  no  further  use  for  money.  These  are  but 
crude  examples.  Prolonged  observations  will  be  necessary,  after 
the  war,  to  estabhsh  the  frequency,  character,  and  permanence  of 
psychical  changes  following  frontal  lesions.  Many  patients  with 
extensive  frontal  destruction  show  no  abnormal  signs  whatever, 
either  physical  or  mental.  It  is  relatively  common,  however,  for 
a  patient  with  a  frontal  wound,  in  the  absence  of  all  other  physical 
or  psychical  abnormalities,  to  have  prolonged  incontinence  of  urine. 
Thus,  in  the  patient  shown  in  Fig.  241,  incontinence  of  urine  was  the 
only  abnormahty  that  persisted  when  he  passed  out  of  observation 
six  weeks  after  his  injury. 

Fractures  of  the  anterior  fossa  of  the  skull,  besides  producing 
lesion  of  the  orbital  surface  of  the  superjacent  frontal  lobes,  may 
tear  across  the  olfactory  nerves  at  the  cribriform  plate,  causing 
anosmia.  This  symptom  is  difficult  to  recognise  in  the  early 
days  after  the  injury.  Sometimes  leakage  of  cerebro-spinal  fluid 
from  the  nose  affords  a  clue,  but  the  patient's  mental  state  is 
rarely  sufficiently  alert  to  permit  of  accurate  testing  of  the  function 
of  smell  until  some  time  later,  when  the  acute  cerebral  symptoms 
have  passed  off. 

(6)  Lesions  of  the  temporal  lobe  are  frequently  devoid  of  focal 
symptoms,  since  the  cortical  auditory  centre  in  the  superior  tem- 
poral gyrus,  and  the  cortical  olfactory  and  gustatory  centres  in 
the  uncinate  gyrus,  are  represented  bilaterally,  in  both  temporal 
lobes.  Thus  one  temporal  lobe  may  be  completely  destroyed 
without  producing  focal  signs.  In  certain  left-sided  lesions, 
however,  as  a  result  of  damage  to  the  word-hearing  centre  on  the 
upper  or  Sylvian  surface  of  the    superior  temporal   convolution, 


510 


NERVOUS   DISEASES 


we   tave   word-deafness.      This  is   exemplified  by  the   following 
case : — 

A  young  soldier  sustained  a  perforating  scalp  wound  in  the  left 
temporal  region,  the  entry  being  four  inches  vertically  above  the  external 
auditory  meatus,  the  exit  half  an  inch  above  the  posterior  end  of  the 
zygoma  (see  Fig.  254).  A  radiogram  showed  no  fracture  of  the  cranium, 
nor  did  exploration  of  the  bullet-track  reveal  any  bare  bone.  Never- 
theless the  temporal  lobe  had  evidently  been  contused,  for,  when 
examined  a  week  after  the  injury,  he  had  a  moderate  degree  of  sensory 
aphasia.  He  spoke  slowly  and  with  difficulty,  occasionally  jumbling 
his  syllables.     He  could  read  aloud  when  shown  written  messages,  but 


Fig.  254. — Tangential  wound  of  left  temporal  region  with 
transient  word-deafness. 

did  not  execute  written  requests,  whilst  with  verbal  requests  he  became 
easily  confused.  There  was  no  motor  or  sensory  abnormality  of  the 
face,  tongue,  or  limbs  on  either  side,  and  the  reflexes,  deep  and  super- 
ficial, were  normal  and  equal  on  the  two  sides.  All  his  aphasic  symp- 
toms gradually  cleared  up. 

.(7)  Lesions  of  the  parietal  region  of  the  cortex  produce  their 
chief  symptoms  by  implication  of  the  sensory  centres  which  extend 
backwards  into  it  from  the  post-central  gyrus  in  front,  and  also  by 
affection  of  the  higher  visual  centres  which  extend  a  Httle  way  into 
it  from  behind,  more  especially  the  word-seeing  centre  in  the  angular 
gyrus  on  the  left  side.  In  some  cases,  therefore,  we  find  astereo- 
gnosis  of  the  contra-lateral  hmb  or  limbs  from  an  antero- superior 
lesion  ;   in  others,  word  bhndness  from  a  lesion  of  the  left  angular 


ORGANIC   WAR-LESIONS 


511 


gyrus.  Lesions  situated  between  these  two  regions,  in  a  "  silent 
area  "  of  the  cortex,  may  be  devoid  of  symptoms,  as  in  the  patient 
shown  in  Fig.  255. 

This  patient  sustained  a  tangential  wound  in  the  right  upper 
parietal  region.  Next  day  the  wound  was  explored,  and  a  depressed 
fracture  was  found  beneath  the  scalp  wound.  The  dotted  line  indicates 
the  extent  of  the  bony  gap  resulting  from  the  craniectomy.  When 
examined  eleven  days  after  the  injury  there  was  no  hemianopia  ;  the 
pupils  and  cranial  nerves  were  normal.  There  was  no  sensory  abnor- 
mality of  the  face,  trunk,  or  limbs.    Stereognosis  was  perfect  in  all  the 


Fig.  255. — Wound  of  right  upper  parietal  region. 

limbs.  There  was  neither  weakness,  tremor,  nor  ataxia  of  the  upper 
or  lower  limbs,  whilst  the  reflexes,  deep  and  superficial,  were  normal 
and  equal  on  the  two  sides. 

(8)  Lesions  of  the  cerebellum  are  in  close  proximity  to  the  vital 
medullary  centres,  which  may  be  fatally  injured  by  shock,  even 
without  being  directly  implicated  in  the  destructive  lesion.  Sub- 
tentorial  lesions,  therefore,  are  so  frequently  fatal  that  in  only  a 
small  proportion  of  cases,  chiefly  of  superficial  injuries,  does  the 
patient  survive  to  show  cerebellar  symptoms.  The  following  is 
an  example  of  this  sort  : — 

The  patient  had  a  perforating  bullet-wound  of  the  skull  in  the 
right  cerebellar  region,  entering  below  the  tip  of  the  right  mastoid 


512  NEKVOUS   DISEASES 

process  and  emerging  immediately  to  the  right  of  the  external  occi- 
pital protuberance. 

When  hit,  he  did  not  lose  consciousness,  but  "  spun  round  and 
round  "  and  fell.  On  being  helped  to  his  feet,  he  could  not  walk  alone, 
but  felt  "  drunk  and  giddy."  He  vomited  within  an  hour  of  his  injury, 
and  had  transient  deafness  of  the  right  ear  with  paresis  of  the  right  side 
of  the  face.  Five  days  after  the  injury,  save  for  slight  right-sided  facial 
paresis,  upper  and  lower,  together  with  a  trace  of  unsteadiness  in 
walking,  all  his  symptoms  had  disappeared.  There  was  neither 
nystagmus,  deafness,  ataxia,  dysdiadochokinesia  nor  other  cerebellar 
symptoms. 

Cranial  nerve  lesions  produced  by  war  injuries  do  not  differ 
essentially  from  those  in  time  of  peace.  As  regards  their 
frequency,  compared  with  injuries  of  peripheral  spinal  nerves, 
cranial  nerve  palsies  are  less  common,  despite  the  fact  that  the 
head  is  more  exposed  to  wounds  than  any  other  part  of  the  body. 
This  is  because  so  many  wounds  which,  if  the  patient  had  survived, 
would  have  shown  cranial  nerve  paralysis,  are  rapidly  fatal  from 
injury  to  the  brain. 

Other  Organic  Brain  Lesions  in  War — It  is  not  to  be  ex- 
pected that  war  should  confer  on  the  combatants  any  immunity 
from  the  ordinary  organic  nervous  diseases  which  are  liable  to  occur 
amongst  peaceful  civilians.  Thus  a  soldier  with  syphilitic  or  other 
variety  of  cardio -vascular  disease  is  liable  to  the  ordinary  types 
of  cerebral  arterial  lesions,  such  as  haemorrhage,  thrombosis,  or 
embolism.  Moreover,  organic  diseases  such  as  disseminated 
sclerosis,  dementia  paralytica,  and  cerebral  tumour  (as  in  the  case 
shown  in  Fig.  226),  also  maladies  like  epilepsy  and  paralysis 
agitans,  whose  morbid  anatomy  is  yet  imknown,  are  not  un- 
commonly precipitated  or  aggravated  by  the  physical  and  emotional 
strain  of  warfare. 

Most  of  the  combatants  are  young  and  active  men  who,  having 
already  passed  at  least  one  medical  examination,  would  in  peace- 
time be  regarded  as  selected  lives.  Chronic  cardiac  or  renal  diseases 
are  therefore  usually  excluded  at  the  outset.  Nevertheless,  even 
in  such  individuals,  a  certain  proportion  of  organic  brain  lesions 
are  directly  attributable  to  war  conditions. 

Perhaps  the  most  dramatic  examples  are  those  cases  in 
which,  in  order  to  arrest  hsemorrhage  in  deep  wounds  of  the 
neck,  the  common  or  internal  carotid  artery^ has  to  be^ligatured. 
Many  of  these  patients  recover  without  cerebral  symptoms  ;  others. 


ORGANIC   WAR-LESIONS 


513 


however,  develop  thrombosis  of  the  middle  cerebral  artery  with 
resulting  hemiplegia.  The  following  is  an  illustrative  example 
of  such  an  accident  : — 

A  healthy  young  soldier,  aged  twenty-two,  of  fine  physique,  was 
shot  in  the  right  side  of  the  neck  during  the  glorious  landing  of  the 
AustraUans  at  the  Dardanelles.  The  bullet  entered  through  the  tip 
of  the  right  mastoid  process  and  emerged  through  the  right  upper  lip, 


FiCr.  256. — Showing  entry-wound  below  right  mastoid  process. 
The  area  of  anaesthesia  of  the  right  side  of  the  face  is 
indicated  by  dark  lines.  The  scar  of  operation  for  ligature 
of  the  common  carotid  is  seen  along  the  anterior  border  of 
the  sterno-mastoid. 

carrying  away  part  of  the  upper  jaw.  Furious  bleeding  occurred, 
which  was  temporarily  arrested  on  the  field  by  firm  plugging.  Later 
in  the  day  it  was  found  necessary,  in  order  to  control  the  haemorrhage, 
to  ligature  the  right  common  carotid  artery.  (The  scar  of  the  operation 
wound  can  be  seen  in  Fig.  256.)  Two  days  later,  on  waking  up,  the 
patient  found  himself  completely  hemiplegic  on  the  left  side.  When 
examined  five  weeks  later,  in  one  of  the  base  hospitals,  the  left  face, 
arm,  and  leg  were  completely  paralysed,  with  flaccidity  of  the  affected 
limbs.  There  were  also  well-marked  sensory  changes,  consisting  in 
slight  blunting  to  cotton-wool  touches  in  the  left  forearm  and  left  leg 
below  the  knee,  together  with  loss  of  joint- sense  at  all  joints  of  the  left 
upper  and  lower  limb,  and  astereognosis  of  the  left  hand  and  foot. 
The  deep  reflexes  were  increased  on  the  paralysed  side,  with  ankle 

2  K 


514  NERVOUS   DISEASES 

clonus  ;  there  was  also  absence  of  the  left  abdominal  reflex,  while  the 
left  plantar  reflex  was  extensor  in  type.  Finally,  there  was  an  area 
of  localised  anaesthesia  to  all  forms  of  sensation  on  the  right  side  of 
the  face,  mainly  in  the  territory  of  the  second  division  of  the  trigeminal 
nerve,  obviously  attributable  to  injury  of  that  nerve  from  the  fracture 
of  the  upper  jaw. 

Hemiplegia  from  vascular  obstruction  may  also  occur  as  a  result 
of  cardio -vascular  disease  acquired  in  war. 

Thus  one  patient,  a  lad  of  twenty-two,  who  was  in  hospital  at  the 
time,  suffering  from  an  attack  of  malaria,  developed  complete  right- 
sided  hemiplegia  and  aphasia  with  absolute  suddenness,  when  turning 
over  in  bed.  There  was  no  loss  of  consciousness.  The  presence  of  an 
aortic  systolic  bruit  led  us  to  diagnose  a  cerebral  embolism. 

Another  patient,  aged  twenty-one,  at  the  end  of  a  prolonged  attack 
of  enteric  fever,  suddenly  discovered  himself  unable  to  move  the  left 
arm  and  there  was  moderate  weakness  of  the  left  lower  limb,  which  sub- 
sequently became  complete.  There  was  no  history  of  venereal  disease  ; 
the  urine  was  free  from  abnormal  constituents.  Two  days  after  the 
onset  of  the  weakness  he  was  found  to  have  complete  flaccid  left  hemi- 
plegia. The  diagnosis  of  cerebral  thrombosis  was  made,  and  seemed 
to  be  supported  by  the  lowness  of  the  systolic  blood-pressure,  measiixing 
118  mm.  of  mercury.  A  week  after  the  onset  of  the  hemiplegic  attack 
he  began  to  recover  power  in  the  affected  muscles.  A  few  days  later, 
signs  of  obstruction  of  the  right  femoral  artery  developed,  with  gangrene 
of  the  foot  and  lower  part  of  the  leg.  The  patient  died  2|  weeks  from 
the  onset  of  the  original  hemiplegia.  At  the  autopsy,  instead  of  throm- 
bosis, recent  emboli  were  found,  one  in  the  profunda  artery  of  the 
thigh,  the  other  in  the  left  middle  cerebral  artery,  with  a  small  area 
of  softening  in  the  left  lenticular  nucleus.  The  heart  showed  recent 
ulcerative  endocarditis  of  the  aortic  cusps. 

Ursemic  convulsions  are  sometimes  met  with,  in  patients  brought 
into  hospitals  or  dressing- stations  on  the  field.  The  medical  officer 
must  be  careful  not  to  confound  such  cases  either  with  ordinary 
epilepsy  or  with  epileptiform  fits  from  gross  cerebral  lesions. 

Cerebro-spinal  meningitis,  whether  sporadic  or  epidemic,  is 
usually  easy  of  recognition,  and  the  diagnosis  is  confirmed  by 
examination  of  the  cerebro-spinal  fluid.  Sometimes,  however, 
difficulty  arises  with  cases  of  meningismus,  in  which  with  pyrexia 
we  find  severe  cerebral  symptoms  such  as  headache,  mental  duhaess, 
or  even  coma,  head-retraction,  &c.  Such  cases  can  only  be  diagnosed 
from  meningitis  by  the  examination  of  the  cerebro-spinal  fluid, 
which  proves  to  be  normal.  These  patients  with  meningismus 
have,  in  my  experience,  most  frequently  proved  to  be  suffering 
from  enteric  fever. 


ORGANIC   WAR-LESIONS  515 

Wounds  of  the  Spinal  Cord 

The  spinal  cord,  bathed  and  supported  by  cerebro-spinal  fluid, 
is  enclosed  within  the  dense  theca.  It  is  further  protected  by 
the  strong,  closely-knit  bones  and  ligaments  of  the  vertebral 
column,  which  in  their  turn  are  supported  externally  by  thick 
masses  of  muscle.  Nevertheless,  war  injuries  of  the  spinal  cord, 
Cauda  equina,  and  spinal  meninges  are  fairly  common.  Injuries 
of  this  sort  are  most  often  caused  by  projectiles  ;  bayonet-wounds 
and  sword-cuts  are  rare. 

Spinal  injuries,  identical  with  accidents  occurring  in  civil  life 
amongst  miners  and  others,  are  also  produced  in  war  by  the  falling 
of  heavy  sandbags  upon  the  vertebral  column,  or  by  the  collapse 
of  trench  walls  or  buildings  mider  shell  or  bomb  explosions. 

Injuries  of  the  spinal  cord  by  bullets  differ  in  some  respects 
from  those  produced  by  fracture-dislocations.  In  bullet-injuries 
the  spinal  cord  may  be  damaged  directly  by  the  penetrating  missile, 
or,  more  commonly,  it  may  be  lacerated  or  compressed  by  in-driven 
fragments  of  bone.  Still  more  frequently  the  bullet-track  passes 
through  or  near  to  the  vertebral  column  without  touching  the 
theca,  and  yet,  notwithstanding  the  absence  of  any  gross  vertebral 
fracture,  severe  spinal-cord  lesions  are  produced  indirectly,  by  the 
concussion  effects  of  the  high -velocity  missile. 

The  pathological  changes  found  in  wounds  of  the  spinal  cord  are 
of  various  types.  Contrary  to  what  might  have  been  expected, 
the  commonest  lesion  is  not  a  haemorrhagic  one,  but  an  area  or 
areas  of  acute  necrosis.  The  spinal  cord  undergoes  sudden  soften- 
ing in  one  or  more  consecutive  segments,  and  there  is  oedematous 
swelling  above  and  below  the  necrotic  zone.  In  a  small  proportion 
of  cases  we  find  a  single  large  intra-medullary  hcemorrhage,  identical 
with  that  which  occurs  in  ordinary  fracture-dislocations.  This 
haemorrhage  extends  upwards  and  downwards  from  the  primary 
lesion,  chiefly  in  the  grey  matter,  the  posterior  horns  and  their 
vicinity  being  more  affected  than  the  anterior  columns.  In  other 
cases  multiple  capillary  hcemorrhages  are  present,  here  again  chiefly, 
though  not  exclusively,  in  the  grey  matter.  In  hgemorrhagic 
lesions  of  the  cord,  whether  large  or  small,  blood  is  usually  effused 
outside  the  cord  as  well,  staining  the  cerebro-spinal  fluid,  in  which 
it  can  be  recognised  by  lumbar  puncture.  Extra-thecal  haemorrhage 
may  also  occur,  sometimes  of  considerable  vertical  extent. 


516  NERVOUS   DISEASES 

In  another  class  of  cases  the  cord  is  compressed  from  without 
by  fragments  of  bone,  by  bullets,  or  still  less  frequently  by 
massive  extra-medullary  haemorrhage. 

Infective  meningo-myelitis  sometimes  supervenes.  This  con- 
dition, developing  at  a  short  interval  after  the  injury,  is  produced 
by  organisms  which  gain  access  to  the  meninges,  usually  through 
a  septic  bullet-track.  Less  commonly  it  is  the  terminal  result  of 
a  deep,  sloughing  bed-sore,  implicating  the  spinal  theca.  It  is 
easily  recognised  by  the  presence  of  root-pains,  muscular  rigidity, 
and  pleocytosis  of  the  cerebro- spinal  fluid.  Meningo-myehtis 
which  spreads  in  an  upward  direction  from  the  level  of  the  original 
lesion  may  mislead  the  observer  by  causing  him  to  locate  the 
primary  lesion  too  high  up.  In  such  cases  radiography  is  of  special 
value,  since  the  question  of  surgical  intervention  for  the  removal 
of  a  septic  bullet  or  of  a  displaced  bony  fragment  should  be  deter- 
mined not  merely  by  the  level  of  the  ansesthesia,  but  by  the  posi- 
tion of  the  vertebral  lesion. 

In  every  spinal  injury,  the  first  problem  to  be  solved  is  whether 
an  organic  lesion  of  the  cord  is  present  or  not.  This  is  usually 
easy  to  determine,  although  functional  paraplegia  may  deceive 
the  unwary,  as  in  the  following  example  : — 

A  soldier,  aged  thirty-six,  was  waiting  in  a  support  trench,  when 
a  shell  landed  close  by.  Its  explosion  blew  him  three  or  four  yards 
along  the  trench.  No  wound  of  the  trunk  was  produced.  He  was 
dazed  for  about  half  an  hour,  but  not  unconscious.  On  being  propped 
on  his  feet,  he  found  great  difficulty  in  standing,  and  on  sitting  down  had 
difficulty  in  getting  up  again.  His  left  lower  limb  also  felt  subjectively 
numb.  He  was  sent  to  a  base  hospital  as  a  case  of  probable  contusion 
of  the  spinal  cord,  and  the  occurrence  of  precipitancy  of  micturition 
after  the  accident  appeared  further  to  lend  support  to  this  diagnosis. 

When  examined  eight  days  after  the  accident,  there  was  no  abnor- 
mality save  in  the  lower  limbs.  The  left  leg  showed  slight  comparative 
blunting  of  sensation  to  all  forms  of  cutaneous  stimulation,  from  the 
knee  downwards.  Joint-sense,  however,  was  unaffected.  He  was 
unable  to  sit  up  without  using  his  hands,  although  the  abdominal 
muscles  contracted  normally.  Both  lower  limbs  were  slightly  feeble, 
especially  the  left,  but  no  movement  was  impossible.  The  gait  was 
typically  functional  in  type.  The  patient  walked  cautiously,  pushing  the 
left  foot  forwards  and  then  dragging  the  right  foot  up  to  it.  The  knee- 
jerks  were  only  just  present ;  the  ankle-jerks  were  brisk  and  equal.  The 
plantar  reflexes  were  of  the  normal  flexor  type  ;  the  abdominal  reflexes 
were  brisk.  There  was  no  spinal  rigidity  or  deformity.  Under  treatment 
by  suggestion,  the  weakness  of  the  legs  rapidly  disappeared,  the  "  stock- 
ing "anaesthesia  cleared  up,  and  the  patient  became  able  to  walk  normally. 


ORGANIC   WAR-LESIONS  5J7 

Should  the  signs  point  to  an  organic  lesion  of  the  spinal  cord, 
we  have  to  determine  the  level  of  the  lesion  and  to  decide  whether 
it  is  complete  or  incomplete.  In  the  case  of  an  incomplete  lesion 
we  have  further  to  consider  whether  it  is  caused  by  extra-medullary 
pressure.  This  may  be  produced  by  a  bullet,  a  fragment  of  shell 
or  in-driven  bone,  or  by  a  large  extra-thecal  haemorrhage,  in  which 
cases  the  possibility  of  operation  for  the  relief  of  such  pressure 
may  have  to  be  considered. 

The  diagnosis  of  the  level  of  a  spinal-cord  lesion  depends  on 
the  accurate  observation  of  the  various  sensory  and  motor  pheno- 
mena.    Let  us  consider  the  sensory  phenomena  first : — 

Two  varieties  of  sensory  disturbance  may  be  present  in  spinal- 
cord  lesions — firstly,  those  due  to  lesion  of  the  posterior  root  (or 
roots)  interrupted  at  the  level  of  the  lesion,  causing  root-ansesthesia 
or  root-hyperaesthesia  ;  and  secondly,  the  sensory  affections  re- 
sulting from  lesion  of  the  sensory  tracts,  which  have  been  damaged 
within  the  spinal  cord. 

A.  Posterior  Root  Symptoms. — Figs.  25  and  26  indicate  the 
cutaneous  distribution  of  the  various  posterior  roots.  In  lesions 
implicating  the  posterior  roots  before  they  have  entered  the  spinal 
cord,  all  forms  of  cutaneous  sensation  are  affected,  and  there  is 
total  anaesthesia  of  the  affected  root-areas.  The  posterior  root 
fibres  may  also  be  damaged  after  they  have  entered  the  spinal  cord, 
but  before  they  have  been  regrouped  to  join  the  various  afferent 
tracts  shown  in  Fig.  12.  In  cases  of  this  sort,  certain  forms  of 
sensation  may  escape,  so  that  the  area  of  loss  to  hght  touches  may 
no  longer  be  co-terminous  with  that  for  pain  or  temperature. 
Further,  the  area  of  cutaneous  loss  is  no  longer  strictly  hmited  to 
a  definite  root-area,  but  may  include  parts  of  several  adjacent 
root-areas.  This  is  better  seen  when  the  hmbs  are  affected,  than 
with  root  lesions  of  the  trunk. 

There  may  also  be  cutaneous  hyperaesthesia  in  the  affected  root- 
area.  In  a  unilateral  lesion  this  hyperaesthesia  occurs  at  the  upper 
margin  of  the  sensory  loss,  on  the  same  side  as  the  spinal-cord 
injury.  It  is  probably  due  to  inflammatory  reaction  or  oedema  of 
the  affected  root  fibres,  whether  outside  or  within  the  spinal  cord. 
It  is  usually  a  transient  phenomenon,  clearing  up,  as  a  rule,  in  a 
few  weeks.  In  some  cases  there  may  also  be  spontaneous  subjective 
root-pains,  whether  running  along  the'  limbs  or  occurring  as  girdle- 
pains  around  the  trunk. 


518  NERVOUS    DISEASES 

B.  Intra-medullary  Sensory  Phenomena. — In  a  complete 
transverse  lesion  all  forms  of  sensation  are  abolished  below  the 
level  of  the  lesion.  In  cases  in  wliicli  the  posterior  roots  are 
implicated  as  well  as  the  spinal  cord  proper,  no  difficulty  arises 
in  the  diagnosis  of  the  level  of  the  injury,  since  the  "  tract 
ansesthesia  "  due  to  interruption  of  the  intra- spinal  sensory  tracts 
is  continuous  with  the  root  ansesthesia. 

Sometimes,  however,  a  transverse  lesion  is  entirely  intra- 
medullary, e.g.  in  acute  necrosis  or  haemorrhage  within  the  spinal 
cord,  and  does  not  implicate  the  posterior  roots  which  enter  at 
that  level.  In  such  a  case  we  no  longer  have  a  root  anaesthesia 
to  guide  us,  but  have  to  deal  with  sensory  loss  resulting  from 
interruption  of  the  various  intra-spinal  tracts.  Owing  to  the 
obliquity  with  which  the  sensory  fibres,  after  entering  one  side  of 
the  spinal  cord,  cross  over  to  the  opposite  spino -thalamic  tract 
(requiring  several  successive  segments  before  their  decussation  is 
complete),  the  upper  border  of  the  ansesthesia  is  lower  than  if  these 
fibres  crossed  horizontally.  This  is  best  observed  in  unilateral 
lesions,  in  which  an  apparent  discrepancy  may  seem,  at  first  sight, 
to  exist  between  the  upper  level  of  the  motor  phenomena  on  one 
side  of  the  body  and  that  of  the  sensory  loss  on  the  opposite  side. 
The  obliquity  of  decussation  of  the  sensory  fibres  is  greatest  in  the 
cervical  region,  where  five  or  six  segments  may  be  required  before 
the  crossing  is  completed,  whereas  in  the  thoracic  region  the  decus- 
sation is  achieved  within  a  single  segment  above  the  level  of  entry 
of  the  posterior  root  fibres.  Unless  these  facts  are  borne  in  mind, 
if  we  depend  on  the  upper  level  of  the  sensory  loss  to  locahse  an 
intra-medullary  lesion,  we  are  liable  to  locate  it  several  segments 
too  low,  especially  if  it  be  in  the  cervical  region,  where  thermal 
sensations  seem  to  cross  within  three  or  four  segments,  painful 
sensations  in  about  four  segments,  and  tactile  sensations  still  more 
obliquely.  Thus  the  upper  margin  of  the  analgesia  and  therm- 
anaesthesia  tends  to  be  slightly  higher  than  that  of  the  tactile  loss. 

Certain  motor  phenomena  are  also  of  great  value  in  localising 
the  level  of  a  spinal-cord  lesion.  They  are  of  two  varieties. 
Firstly,  we  have  segmental  motor  signs,  due  to  injury  of  the  anterior 
cornua  or  anterior  roots  at  the  level  of  the  lesion  ;  and  secondly, 
pyramidal  signs,  due  to  injury  of  the  antero -lateral  columns  of  the 
cord. 

The  segmental  innervation  of  the  muscles  of  the  neck,  upper 


ORGANIC   WAR-LESIONS  519 

and  lower  limbs,  is  well  known,  and  is  indicated  in  the  tables  on 
p.  41.  In  the  thoracic  region  of  the  cord,  between  the  lower  end 
of  the  cervical  and  the  upper  end  of  the  lumbar  enlargement,  each 
segment  innervates  its  corresponding  intercostal  muscle,  together 
with  a  portion  of  the  spinal  and  abdominal  muscles  at  that  par- 
ticular level,  the  rectus  abdominis  corresponding  to  the  segments 
from  the  6th  to  the  10th  thoracic,  and  the  obliquus  abdominis 
to  the  lowest  two  thoracic  segments. 

Bearing  these  facts  in  mind,  it  is  comparatively  easy  to  identify 
the  particular  segment  (or  segments)  of  the  cord  in  which  there 
has  been  a  lesion  of  the  anterior  comua  or  anterior  roots,  inasmuch 
as  the  muscles  corresponding  to  that  segment  (or  segments)  undergo 
atrophic  paralysis  and,  after  a  week  or  ten  days,  show  the  elec- 
trical reactions  of  degeneration.  Thus  in  lesions  afEecting  the 
cervical  or  lumbar  enlargements  we  fuid  certain  groups  of  muscles 
in  the  limbs  marked  out  from  the  others,  whereas  in  lesions  of  the 
thoracic  region  the  paralysed  intercostal  muscles  can  readily  be 
differentiated  from  the  non-paralysed  intercostals  higher  up,  by 
palpation  and  sometimes  even  by  inspection.  Lesions  of  the  ninth 
thoracic  segment  produce  paralysis  of  the  lower  part  of  the  recti 
abdominis,  whilst  the  upper  halves  of  the  recti  remain  unaffected ; 
hence,  when  the  patient  attempts  to  sit  up,  the  umbilicus  is  drawn 
upwards.  Lesions  of  the  11th  thoracic  segment  spare  the  recti  alto- 
gether, but  the  obliquui  abdominis,  in  the  flanks,  are  paralysed. 

Pyramidal  motor  signs,  characteristic  of  an  upper  motor  neurone 
lesion,  are  already  familiar,  and  need  not  here  be  discussed  in  detail. 
It  should  be  remembered  that  in  all  severe  traumatic  lesions  of  the 
spinal  cord  the  paralysed  lower  limbs  are  at  first  flaccid,  with  absent 
ankle-jerks  and  knee-jerks.  If  the  lesion  be  a  complete  transverse 
one,  the  muscles  remain  flaccid  and  the  deep  reflexes  do  not  re- 
appear. If  the  lesion  be  incomplete,  the  muscles  regain  their  tone, 
and  within  two  or  three  weeks  rigidity  sets  in,  sometimes  accom- 
panied by  reflex  flexor  spasms,  whilst  the  deep  reflexes  reappear 
and  become  exaggerated,  giving  the  typical  clinical  picture  of  an 
upper  motor  neurone  lesion.  In  unilateral  lesions  the  deep  reflexes 
in  the  ipso-lateral  paralysed  lower  limb  are  diminished  or  lost  for 
the  fijst  week  or  two,  subsequently  proceeding  to  the  stage  of 
exaggeration. 

Is  the  Transverse  Lesion  Complete  or  Incomplete? — In 
complete  transverse  lesions  the  plantar  reflexes  are  at  first  absent. 


520  NERVOUS   DISEASES 

In  a  week  or  two,  however,  they  reappear  and  are  of  an  extensor 
type.  In  some  cases,  in  which  the  transverse  lesion  is  probably 
incomplete,  feeble  plantar  reflexes  of  flexor  type  can  be  elicited 
from  the  outset,  giving  place,  after  two  or  three  weeks,  to  the 
classical  Babinski  extensor  response. 

If  the  lesion  be  a  complete  one,  with  total  functional  discon- 
tinuity of  the  upper  from  the  lower  fragment  of  the  spinal  cord, 
the  damage  is  irreparable,  and  inasmuch  as  regeneration  of  nerve 
tissues  does  not  occur  within  the  central  nervous  system,  no  opera- 
tion— e.g.  for  the  removal  of  a  projectile  or  of  a  displaced  fragment 
of  bone,  if  present — is  likely  to  be  of  any  avail. 

In  some  cases  of  transverse  lesion,  the  spinal  cord  is  anatomically 
severed,  so  that  there  is  a  gap  between  the  upper  and  lower  seg- 
ments. More  often,  however,  it  is  only  physiologically  interrupted, 
from  disintegration  of  the  nervous  tissues  at  the  level  of  the  injury. 
In  both  varieties  the  clinical  result  is  the  same  :  the  patient  has 
complete  flaccid  paraplegia  with  anaesthesia  below  the  level  of  the 
lesion,  together  with  permanent  loss  of  the  ankle- jerks  and  knee- 
jerks.  The  plantar  reflexes  are  usually  absent  at  first,  but  may 
return  later,  assuming  the  extensor  type.  In  other  cases,  in 
which  a  shred  of  nervous  tissue  survives,  joining  the  segments 
above  the  lesion  to  those  below  it,  the  motor  and  sensory  paralysis 
is  complete,  but  the  deep  reflexes  gradually  return  and  become 
exaggerated,  whilst  the  plantar  reflexes  become  extensor  in  type. 

In  a  transverse  lesion  confined  to  a  single  segment  of  the  spinal 
cord,  the  muscles  corresponding  to  that  segment  undergo  atrophic 
paralysis  with  loss  of  faradic  excitability,  as  already  described, 
whereas  the  paralysed  muscles  corresponding  to  all  the  segments 
lower  down,  usually  retain  their  electrical  reactions.  In  a  certain 
proportion  of  cases,  however,  all  the  paralysed  muscles,  from  the 
level  of  the  lesion  downwards,  lose  their  faradic  excitability  within 
a  week  or  ten  days  after  the  original  injury.  This  loss  of  response 
remains  permanent.  So  far  as  I  have  been  able  to  judge,  in  a 
series  of  eight  cases  with  injuries  at  various  levels,  from  the 
cervical  region  downwards,  the  lesion  in  each  of  them  was  an  acute 
softening,  not  a  severance  of  the  spinal  cord  by  direct  injury. 
The  probable  explanation  is  to  be  sought  in  molecular  changes 
occurring  in  all  the  anterior  cornual  cells  from  the  level  of  the 
lesion  downwards. 

Let  us  first   consider  those    cases    in   which  a    lesion    causes 


ORGANIC   WAR-LESIONS 


521 


complete  interruption  of  the  spinal  cord,  whether  directly  by  the 
bullet  track  or  indirectly  by  concussion  necrosis.  In  a  recent 
series  of  thirty-four  personally  observed  cases  (exclusive  of  cauda 
equina  lesions),  the  signs  pointed  to  a  complete  transverse  lesion 
in  seventeen,  i.e.  in  one  half  of  the  cases.  The  following  is  an 
example  of  direct  bullet  injury  : — 

A  soldier,  aged  twenty-four,  was  wounded  by  a  rifle  bullet  which 
entered  one  inch  above  the  middle  of  the  rijjht  clavicle  and  came 
out  one  and  a  half  inches  above  the  middle  of  the  left  clavicle.     He 
immediately  lost  power  and  sensation  in  the  trunk 
and  lower  limbs.    There  was  persistent  retention 
of  urine,  for  which  the  catheter  had  been  used. 

When  examined,  five  days  after  the  injury,  the 
patient  had  complete  angesthesia  to  all  forms  of 
cutaneous  stimulation  up  to  the  level  of  the  2nd 
ribs  in  front  and  to  the  2nd  thoracic  spine  behind, 
also  along  the  inner  margins  of  both  upper  limbs, 
in  the  distribution  of  the  7th  and  8th  cervical  and 
1st  thoracic  segments  (see  Fig.  257).  Vibration 
sense  was  lost  in  the  lower  limbs  and  trunk,  up 
to  the  3rd  thoracic  spine,  also  in  the  two  ulnar 
fingers  of  the  right  hand.  Joint-sense  was  absent 
in  the  lower  limbs  and  impaired  in  the  fingers  of 
both  hands. 

The  motor  functions  of  the  head,  neck,  dia- 
phragm, and  upper  limbs  were  normal,  with  the 
exception  of  the  intrinsic  muscles  of  the  hands, 
which  were  paralysed.  The  intercostal  and  ab- 
dominal muscles  were  paralysed,  together  with  the 
spinal  muscles,  and  there  was  total  flaccid  paraplegia 
of  both  lower  limbs.  The  knee-jerks  and  ankle- 
jerks  were  absent,  as  also  were  the  plantar  and  abdominal  reflexes.  All 
the  muscles  of  the  trunk  and  upper  and  lower  limbs  reacted  normally 
to  faradism.  There  was  retention  of  urine  with  overflow  incontin- 
ence. The  urine  was  ammoniacal  and  contained  pus.  The  cerebro- 
spinal fluid  was  bloodstained,  and  on  standing  yielded  a  supernatant 
deep  yellow  fluid  with  a  gelatinous  coagulum.  The  temperature  was 
moderately  raised,  to  101-4°  F.  A  superficial  bed-sore  was  present 
over  the  sacrum. 

The  patient  died  sixteen  days  after  the  date  of  injury.  At  the 
autopsy  the  bullet  track  was  found  to  have  traversed  the  spinal  cord 
at  the  level  of  the  8th  cervical  segment,  the  upper  and  lower  frag- 
ments of  the  cord  being  joined  only  by  a  thin  strip  of  tissue  in  front 
of  the  anterior  commissure.  A  small  piece  of  bone  was  embedded  in 
the  inner  surface  of  the  theca  at  the  left  side,  having  been  carried 
through  from  right  to  left.  No  haemorrhage  could  be  seen,  by  the 
naked  eye,  in  the  substance  of  the  spinal  cord  above  or  below  the  level 


Fig.  257.— Total 
transverse  lesion 
at  level  of  8th 
cervical  segment. 


522  NERVOUS   DISEASES 

of  the  injury,  nor  was  there  any  hole  visible  in  the  spinal  theca, 
although  the  bullet-track  in  the  spinal  cord  and  the  bony  fragment 
within  the  dura  mater  showed  that  it  must  have  been  perforated. 

The  next  case  is  one  of  acute  softening  from  concussion 
necrosis  :— 

An  officer,  aged  thirty-five,  was  wounded  by  a  bullet  whose  aperture 
of  entry  was  one  inch  to  the  left  of  the  9th  thoracic  spine,  the  exit 
being  in  the  right  mid-axillary  line,  between  the  8th  and  9th 
ribs.  When  examined  five  days  later,  in  addition  to  the  signs  of  a 
right-sided  hgemothorax,  there  was  total  flaccid  paralysis  of  the  lower 
limbs  and  of  the  lower  abdominal  muscles,  the  umbilicus  being  pulled 
upwards  when  the  patient  attempted  to  sit  up.  There  was  anaesthesia 
of  the  lower  limbs  and  trunk,  to  all  forms  of  stimuli,  up  to  a  level 
three  inches  above  the  pubes.  The  knee-jerks  and  ankle-jerks  were 
absent,  also  the  bulbo-cavernosus,  plantar,  and  abdominal  reflexes. 
There  was  retention  of  urine  with  overflow'incontinence.  The  cerebro- 
spinal fluid  was  clear  and  showed  no  abnormality  on  microscopic 
examination. 

The  patient  died  on  the  twenty-first  day  after  the  injury.  At  the 
autopsy  the  spinal  theca  was  uninjured,  and  no  haemorrhage  was  present, 
either  inside  or  outside  it.  At  the  level  of  the  12th  thoracic  segment 
the  spinal  cord  was  soft  and  pulpy  for  a  vertical  extent  of  about  an 
inch.  After  suitable  hardening,  sections  through  the  softened  area 
showed  that  the  damage  was  mainly  in  the  posterior  region  of  the  cord, 
implicating  both  grey  and  white  matter.  Microscopic  examination 
showed  simple  disintegration  of  the  nervous  elements,  with  moderate 
proliferation  of  small  round  cells.  There  was  no  evidence  of  haemor- 
rhage, old  or  recent. 

Incomplete  transverse  lesions  of  the  spinal  cord  are  some- 
times mainly  unilateral.  Such  cases,  occurring  above  the  lumbar 
enlargement,  produce  the  Brown-Sequard  syndrome,  consisting  in 
motor  paralysis  on  the  ipso-lateral  side,  with  dissociated  anaesthesia 
on  the  contra-lateral  side,  as  in  the  following  example  : — 

The  patient,  a  bandsman,  was  wounded  by  a  shrapnel-bullet  which 
entered  the  right  side  of  the  neck  at  the  middle  of  the  anterior  border 
of  the  sterno-mastoid  muscle.  There  was  no  wound  of  exit.  The 
bullet  crossed  the  middle  line  and  lodged  close  behind  the  outer  end  of 
the  left  clavicle,  where  it  was  discovered  by  radiographic  examination 
three  weeks  later.  When  wounded,  the  patient  fell  to  the  ground 
powerless  in  all  his  limbs.  In  a  few  minutes  he  found  himself  able 
to  move  the  right  arm,  and  next  day  he  recovered  some  power  in  the 
right  leg.  There  was  some  delay  in  micturition,  but  catheterisation 
was  never  required. 

When  examined  six  days  after  the  injury,  the  right  pupil  was  slightly 


ORGANIC   WAR-LESIONS 


523 


larger  than  the  left.     Both  pupils  reacted  normally,  and  the  cranial 
nerves  were  otherwise  normal. 

To  cotton-wool  touches  there  was  anaesthesia  of  the  feet  and  ankles 
up  to  the  junction  of  the  lower  and  middle  thirds  of  the  legs.  To 
pain  and  temperature  there  was  loss  of  sensation  in  the  right  lower 
limb  and  right  half  of  the  trunk  up  to  the  level  of  the  3rd  rib,  extend- 
ing along  the  inner  side  of  the  right  upper  limb  in  the  distribution 
of  the  7th  and  8th  cervical  and  first  thoracic  root  -  areas  (see 
Fig.  258).  This  analgesia  and  therm-anaesthesia  also  extended  across 
the  middle  line  of  the  trunk  in  a  zone  from  the  3rd  rib  to  just  below 
the  nipple,  and  along  the  inner  side  of  the  left  upper  limb  in  a  distri- 
bution similar  to  that  on  the  right  side.  Joint-sense 
was  normal  in  the  lower  and  U])per  limbs,  except  in 
the  two  ulnar  digits  of  the  left  hand,  in  which  it  was 
deficient.  Vibration  sense  was  lost  in  the  lower 
limbs  and  lower  part  of  the  trunk,  up  to  the  level 
of  the  5th  thoracic  spine. 

The  left  lower  limb  was  completely  paralysed 
and  flaccid.  The  right  lower  limb  could  be  volun- 
tarily moved  at  all  joints.  The  abdominal  and 
intercostal  muscles  were  paralysed  on  both  sides  ; 
the  diaphragm  moved  normally. 

In  the  right  upper  limb  there  was  paralysis  of 
all  the  intrinsic  hand  muscles  and  of  the  long 
flexors  and  extensors  of  the  fingers  and  thumb, 
whilst  the  movements  of  the  wrist,  forearm,  elbow, 
shoulder,  and  scapula  were  normal.  In  the  left 
upper  limb  there  was  paralysis  of  the  intrinsic  hand 
muscles  and  of  all  the  flexors  and  extensors  of  the 
fingers  and  wrist  (except  the  extensor  carpi  radialis 
brevior).  The  triceps  was  also  paralysed.  All  the 
other  muscles  of  the  limb  were  normal. 

The  head  and  neck  moved  normally. 

The  biceps-jerks  in  the  upper  limbs  were  brisk; 
the  triceps- jerks  were  absent. 

In  the  right  lower  limb  the  knee-jerk  was  brisk,  the  ankle-jerk  feeble. 
In  the  left  lower  limb  the  knee-jerk  and  ankle-jerk  were  absent. 

The  right  plantar  reflex  was  flexor  in  type,  the  left,  at  this  stage,  was 
absent.  A  week  later  the  left  plantar  reflex  was  definitely  extensor 
in  type. 

The  abdominal  reflexes  were  absent. 

Beyond  slight  delay  in  micturition,  the  sphincters  were  otherwise 
normal. 

The  right  side  of  the  head  and  neck,  with  the  right  upper  thoracic 
wall,  were  noticed  to  sweat  excessively. 

Gradual  improvement  set  in.  A  week  later  the  right  rectus  ab- 
dominis was  observed  to  have  regained  voluntary  power,  whilst  the 
left  thigh  muscles  were  also  beginning  to  recover.  When  the  patient 
passed  out  of  observation  six  weeks  after  his  injury,  the  cotton-wool 


Fig.  258. — Incom- 
plete transverse 
lesion  at  level  of 
8th  cervical  seg- 
ment. Brown- 
Sequard  syn- 
drome. 


524 


NERVOUS   DISEASES 


ansesttiesia  had  disappeared,  whilst  the  analgesia  and  therm-anaesthesia 
were  unchanged.  The  left  lower  limb  had  regained  motor  power  at 
all  joints,  but  was  still  considerably  feebler  than  the  right.  The  ab- 
dominal muscles  contracted  on  both  sides,  the  right  better  than  the 
left.  The  intercostal  muscles  still  remained  paralysed.  In  the  right 
upper  limb  no  individual  muscle  was  now  paralysed.  In  the  left 
upper  limb  the  intrinsic  muscles  of  the  hand  had  recovered.  The  tri- 
ceps contracted  feebly,  also  the  extensors  of  the  wrist.  The  only 
muscles  that  remained  totally  paralysed  were  the  long  flexors  and 
extensors  of  the  fingers.  The  knee-jerks  were  brisk,  also  the  ankle- 
jerks.  There  was  now  left-sided  ankle -clonus,  and  both  plantar 
reflexes  were  now  extensor  in  type. 

An  incomplete  transverse  lesion  of  the  spinal  cord  may  involve 
mainly  the  mesial   or    central  region  of   the    cord,   leaving  un- 


FiG.  259. — Incomplete  transverse  lesion  with  escape  of  lower 
sacral  root-areas. 

damaged  the  fibres  nearer  the  surface.  Inasmuch  as  the  spino- 
thalamic fibres  (conveying  sensations  of  temperature  and  pain) 
corresponding  to  the  lowest  spinal  roots,  lie  nearest  the  surface 
of  the  lateral  columns,  the  result  is  that  the  sacral  cutaneous 
root-areas — i.e.  the  region  of  the  genitals,  perineum,  and  "  saddle 
area  "  of  the  buttocks  and  thighs — tend  to  escape,  whilst  the 
root-areas  higher  up,  corresponding  to  the  more  mesially-situated 
fibres  of  the  spino-thalamic  tract,  are  alone  afiected  by  anaesthesia. 
The  following  is  an  illustrative  case  : — 

The  patient,  aged  twenty,  was  wounded  by  a  bomb  explosion  which 
produced  three  wounds    in   the   back,  all    at  the  level  of  the  12th 


ORGANIC   WAR-LESIONS 


525 


thoracic  spine,  to  the  left  of  the  middle  line.  A  radiogram  showed  a 
bullet  2^  inches  to  the  right  of  the  middle  line  at  the  level  of  the  lOth 
thoracic  spine.  The  patient  at  once  lost  all  power  and  sensation  in 
the  lower  limbs,  and  for  a  week  had  retention  of  urine  requiring  catheter. 
After  a  few  days,  sensation  began  to  return  in  the  lower  limbs,  but  they 
still  remained  powerless. 

When  examined  four  weeks  after  the  injury,  there  was  loss  of  sensa- 
tion to  cotton-wool  touches  in  the  right  lower  limb,  front  and  back, 
as  high  as  the  groin.  To  pin-pricks  and  temperature  there  was  loss 
of  sensation  in  both  lower  limbs  and  in  the  lower  part  of  the  abdomen, 
whilst  an  area  on  the  back  of  the  thighs,  together  with  the  genitals, 
retained  normal  sensation  (see  Fig.  259).  Joint-sense  was  lost  at  the 
toes,  ankles,  and  knees,  normal  at  the  hips. 

The  lower  abdominal  muscles  were  paralysed,  so  that  the  umbilicus 
was  pulled  upwards  on  attempting  to  sit  up.     There  was  total  flaccid 


Fig.  260. — The  same  case  as  Fig.  259,  showing  further 
recovery  of  sacral  root-areas. 

paralysis  of  all  the  muscles  of  the  lower  limbs,  except  of  the  adductors 
of  both  thighs  and  the  left  sartorius,  which  contracted  feebly. 

The  knee-jerks  were  normal ;  there  was  ankle  clonus  on  the  left 
side  only  ;  the  right  ankle-jerk  was  normal.  The  plantar  reflexes 
were  both  extensor  in  type.     The  sphincters  were  normal. 

The  cerebro-spinal  fluid  was  clear  and  colourless,  containing  one 
lymphocyte  per  cubic  millimetre. 

The  signs  and  symptoms  gradually  improved,  so  that  a  month 
later  (see  Fig.  260)  the  area  of  analgesia  and  therm-aneesthesia  had 
further  receded,  and  the  sensory  loss  corresponded  to  the  root-areas 
from  the  12th  thoracic  to  the  5th  lumbar  inclusive,  the  areas  below 
that  level  having  almost  entirely  recovered.  Together  with  this,  there 
was  a  return  of  motor  power  in  all  the  muscles  of  the  lower  limbs, 
although  the  patient  was  not  yet  able  to  walk.     There  was  knee  clonus 


526  NERVOUS   DISEASES 

and  ankle  clonus  on  both  sides,  and  the  plantar  reflexes  were  extensor 
as  before. 

Cases  like  the  foregoing  might  readily  be  confounded  with  lesions 
of'^'ithe  upper  roots  of  the  cauda  equina,  but  are  distinguished  by 
the  evidences  of  medullary  lesion,  such  as  increase  of  the  knee- 
and  ankle- jerks  with  the  presence  of  clonus,  the  extensor  type  of 
plantar  reflexes,  and  the  absence  of  muscular  atrophy. 

Much  less  frequently  an  incomplete  transverse  lesion  spares 
the  antero -lateral  columns  and  damages  mainly  the  posterior 
columns.  If  such  a  lesion  is  above  the  cervical  enlargement,  the 
residual  signs  are  those  of  ataxia  of  the  upper  and  lower  limbs 
without  motor  paralysis,  but  with  loss  of  joint-sense  and  vibration- 
sense  (both  of  which  are  conducted  upwards  exclusively  in  the 
posterior  columns).  The  superficial  reflexes  remain  normal,  whilst 
the  deep  reflexes  are  diminished  or  lost. 

We  may  also  have  shght  contusion  with  transient  oedema  of 
the  spinal  cord  without  anatomical  interruption  of  any  of  its  fibres. 
In  such  cases  the  patient,  after  an  initial  stage  of  total  paraplegia, 
makes  a  good  recovery,  as  in  the  following  example  : — 

A  young  officer,  aged  twenty-one,  had  a  bullet  wound  which  entered 
IJ  inches  to  the  left  of  the  middle  line  at  the  level  of  the  7th  cervical 
spine.  The  exit  was  immediately  behind  the  right  sterno-mastoid 
muscle,  Ih  inches  below  the  tip  of  the  mastoid  process. 

When  hit,  the  patient  immediately  fell  forwards,  but  with  the 
sensation  of  falling  very  slowly.  He  was  not  unconscious.  At  first 
he  was  unable  to  move  any  limb,  but  within  a  few  minutes  he  found  he 
could  move  his  head  freely.  Within  a  day  motor  power  began  to  return 
in  all  the  limbs,  except  the  right  upper  extremity.  There  was  no 
sphincter  trouble  from  the  outset.  When  admitted  on  the  second  day 
to  a  hospital  ship,  he  was  found  to  be  suffering  also  from  a  mild  degree 
of  trench-feet,  resulting  from  exposure  to  cold  and  damp  after  being 
wounded.  Both  feet  were  swollen,  especially  the  right  foot,  and  the 
right  hallux  shortly  developed  a  small  black  necrotic  area  at  the  tip 
of  its  distal  phalanx. 

On  examination  thirteen  days  after  the  injury,  the  pupils  and  cranial 
nerves  were  normal.  To  cotton-wool  touches  there  was  comparative 
blunting  of  sensation  along  the  inner  side  of  the  right  upper  limb 
(see  Fig.  261),  including  1|  ulnar  fingers.  To  pin-pricks  there  was  no 
loss  in  the  upper  limbs  or  trunk,  but  in  the  feet  there  was  total  analgesia 
up  to  3  inches  above  the  ankles.  Vibration-sense  was  everywhere 
normal.     Joint -sense  was  lost  in  the  right  little  finger  only. 

In  the  right  upper  limb  there  was  total  paralysis  of  the  triceps, 
extensors  of  the  wrist,  fingers  and  thumb,  and  of  all  the  intrinsic  hand 
muscles.     The  supinator  longus  and  latissimus  dorsi  were  paresed  ; 


ORGANIC   WAR-LESIONS 


527 


all  the  other  muscles  of  the  limb  were  normal.  The  left  upper  limb, 
together  with  the  diaphragm,  intercostals,  spinal  and  abdominal 
muscles,  and  the  muscles  of  the  lower  limbs,  were  normal  in  their  move- 
ments, save  for  some  paresis  of  the  toes  and  ankles,  especiallv  on  the 
right  side.     Both  feet,  especially  the  right,  were  ocdematous. 

The  biceps- jerks  and  triceps-jerks  were  absent ;  the  knee-jerks  and 
ankle- jerks  were  brisk.  The  plantar  reflexes  were  absent ;  the  ab- 
dominal reflexes  were  faint.    The  sphincters  were  normal. 

To  faradism  all  the  muscles  of  the  upper  and  lower  limbs  reacted 
briskly,  including  the  paralysed  muscles  of  the  right  upper  limb. 

A  week  later  the  cutaneous  ansesthesia  had  cleared  up  in  the  right 
upper  limb,  although  joint-sense  was  still  absent  in  the  little  finger. 


Fig.  261. — Transient  lesion  of  spinal  cord  in  cervical  region. 
The  patient  also  had  trench-feet. 

The  triceps,  supinator  longus,  and  extensors  of  the  wrist  all  contracted 
feebly  ;  the  extensors  of  the  fingers  were  still  paralysed.  The  biceps- 
jerk  and  triceps-jerk  were  still  absent  in  the  right  upper  limb,  but  had 
reappeared  in  the  left. 

Lesions  of  the  cauda  equina  from  bullet  wounds  tend  to  be  less 
symmetrical  than  civilian  injuries  (see  p.  245),  but  otherwise 
present  no  essential  difference.  Their  diagnosis  is  usually  easy. 
The  following  are  illustrative  examples  : — 

The  patient,  aged  twenty-four,  was  struck  by  a  shrapnel  bullet 
which  entered  the  back  1^  inches  to  the  right  of  the  middle  Hne  at  a 
level  between  the  second  and  third  lumbar  spines.  He  immediately 
lost  power,  both  motor  and  sensory,  in  the  legs,  and  during  the  fiist 
week  had  intermittent  dribbling  of  urine,  which  subsequently  cleared 
up,  so  that  he  became  able  to  initiate  micturition  by  compression  of 
the  abdominal  muscles.     During  the  first  two  days  after  the  injury 


528 


NERVOUS   DISEASES 


he  had  severe  pains  in  the  calves  of  the  legs.    A  radiogram  showed 
the  shrapnel  bullet  within  the  body  of  the  second  lumbar  vertebra. 

On  examination,  two  and  a  half  weeks  after  the  injury,  there  was 
no  abnormality  save  in  the  lower  limbs.  The  abdominal  muscles  were 
powerful,  and  he  could  sit  up  without  using  the  upper  limbs.  To 
pin-pricks  there  was  total  analgesia  of  the  lower  limbs,  from  the  level 
of  the  third  lumbar  roots  downwards  (see  Fig.  262),  including  the  geni- 
tals. To  cotton-wool  touches  there  was  anaesthesia  in  the  same  area, 
save  in  the  front  of  the  left  thigh  and  knee.  Joint -sense  was  preserved 
in  the  left  hip-joint  and  lost  in  all  other  joints  of  both  lower  limbs. 
Vibration -sense  was  lost  in  the  bones  of  the  lower  limbs,  except  in  the 
left  femur.  There  was  total  flaccid  paralysis  of  both  lower  limbs, 
except  in  the  sartorii,  with  loss  of  faradic  excitability  in  all  the  muscles, 


Fig.  262. — Lesion  of  cauda  equina. 

save  in  the  sartorii  and  in  the  left  quadriceps  extensor.  The  knee- 
jerks  and  ankle-jerks  were  absent,  also  the  plantar,  bulbo-cavernosus, 
and  superficial  anal  reflexes.  The  abdominal  reflexes  were  brisk. 
There  was  a  healed  bed-sore  over  the  sacrum.  A  few  days  later, 
voluntary  power  returned  in  the  left  quadriceps  extensor.  Apart 
from  this,  the  patient's  condition  remained  unchanged,  when  he  left 
for  England  two  weeks  afterwards. 

The  next  case  is  an  example  of  a  right-sided  cauda  equina  lesion 
of  much  more  limited  extent  : — 

The  patient,  aged  twenty-four,  was  wounded  by  a  shrapnel  bullet 
which  entered  IJ  inches  to  the  right  of  the  fourth  lumbar  spine.  A 
radiogram  showed  the  bullet  lodged  between  the  laminse  of  the  third 
and  fourth  lumbar  vertebrae.  When  hit,  both  lower  limbs  immediately 
became  powerless,  but  within  a  few  minutes  he  became  able  to  move 
the  left  limb.     The  movements  of  the  right  hip  and  thigh  also  returned. 


ORGANIC   WAR-LESIONS 


529 


but  the  right  ankle  and  toes  remained  powerless.  He  had  subjective 
tingling  of  the  right  limb  from  the  thigh  downwards,  which  subse- 
quently receded  to  the  right  sole.  There  was  retention  of  urine  for 
the  first  four  days. 

On  examination  three  weeks  after  the  injury,  there  was  no  loss  of 
cutaneous  sensibility  to  cotton-wool  touches,  but  to  pin-pricks  there 
was  a  small  area  of  analgesia  in  the  sole  of  the  right  foot  (see  Fig.  263). 
Joint-sense  and  vibration-sense  were  everywhere  normal. 

The  movements  of  the  left  lower  limb  were  powerful  at  all  joints, 
also  those  of  the  right  hip  and  knee.  There  was  total  paralysis  of  the 
right  peronei,  long  extensors  of  the  toes,  and  tibialis  anticus,  with  drop- 


FlG.  263. — Limited  right-sided  cauda  equina  lesion. 

foot  on  that  side.  The  right  calf-muscles  and  long  flexors  of  the  toes 
were  feeble. 

The  left  knee-jerk  was  brisk,  the  right  absent.  Both  ankle-jerks 
were  absent.  The  left  plantar  reflex  was  brisk  and  of  normal  flexor 
type  ;  the  right  was  absent.  The  cremasteric  reflexes  were  brisk  and 
equal.  The  bulbo-cavernosus  reflex  was  absent.  The  sphincters  were 
now  normal. 

To  faradism  there  was  diminution  of  excitability  in  the  calf 
muscles  and  anterior  tibial  group  on  the  right  side,  but  no  individual 
muscle  failed  to  react.  It  seemed  probable,  therefore,  that  those 
muscles  would  soon  recover.  The  patient  was  transferred  to  England 
a  few  days  later,  and  passed  out  of  observation. 

Tetanus  is  met  with  in  military  practice  much  more  commonly 
than  in  civil  life.  Although  this  disease  is  a  general  iniection,  it  is 
convenient  to  refer  to  it  here,  since  its  chief  symptoms  are  due  to 
irritation  of  the  brain-stem,  especially  of  the  medullary  and  spinal 
motor  nuclei,  by  the  tetanus  toxin. 

2  L 


530  NEEVOUS    DISEASES 

The  tetanus  bacillus  is  anaerobic.  It  gains  entrance  througb 
some  septic  wound,  the  infection  being  almost  invariably  carried 
by  manure-infected  dust  or  soil.  It  flourishes  amongst  the  sloughing 
debris  in  a  lacerated  wound,  where  its  growth  is  favoured  by  the 
presence  of  suppurative  organisms.  The  clinical  symptoms  are 
produced  not  by  the  tetanus  bacillus  directly,  but  by  its  toxin, 
which  spreads  upwards  from  the  muscle  end-plates  along  the  motor 
nerves  to  the  motor  nuclei  of  the  brain-stem.  In  generalised 
tetanus-toxsemia  all  the  muscles  are  poisoned,  but  the  motor  nuclei 
which  have  the  shortest  motor  nerves  are  reached  earliest  by  the 
toxin  and  thrown  into  a  state  of  intense  excitability.  Thus  the  jaw, 
facial  and  cervical  muscles,  are  usually  the  earliest  to  show  tetanic 
spasms  ;  later  the  spinal  and  abdominal  muscles  ;  and  last  of  all 
the  limbs.  Occasional  exceptions  to  this  rule  occur.  The  time 
required  for  the  toxin  to  travel  from  the  end-plates  to  the  motor 
nuclei  constitutes  the  period  of  incubation,  varying  from  a  day 
or  two  to  nearly  three  weeks.  The  longer  the  incubation  period, 
the  better  is  the  prognosis. 

After  a  premonitory  stage  of  general  nervous  irritability  and 
change  of  character,  the  patient  complains  of  stiffness  of  the  muscles 
of  the  neck  or  jaws.  Gradually  a  tonic  spasm  supervenes  in  the 
affected  muscles,  producing  lockjaw,  stiffness  of  the  neck  and  rigid 
spasm  of  the  facial  muscles  {risus  sardonicus),  the  angles  of  the  mouth 
being  drawn  outwards  and  the  eyebrows  raised.  Gradually  the 
trunk  muscles  may  become  affected,  producing  rigidity  of  the  ab- 
domen and  spine.  The  muscular  spasm  varies  in  intensity  from 
time  to  time.  During  the  frequent  paroxysms  of  increased  spasm 
there  may  be  opisthotonos,  head  retraction,  and  aggravation  of  the 
facial  and  mandibular  spasm.  These  paroxysms  last  from  a  few 
seconds  to  several  minutes,  and  even  in  the  intervals  between  them 
the  muscles  do  not  completely  relax.  Slight  stimuli — e.g.  touching 
the  patient,  loud  noises,  bright  light,  &c. — precipitate  the  paroxysms. 
The  muscular  cramps  are  associated  with  intense  pain.  There  is 
no  anaesthesia  nor  true  motor  paralysis.  The  deep  reflexes  are 
increased.  The  patient  sweats  profusely.  His  temperature  may 
be  normal  throughout ;  more  often  there  is  fever,  sometimes  of 
a  high  degree.  In  fatal  cases  death  may  be  due  to  respiratory  or 
larjmgeal  spasm,  to  heart  failure,  or  to  exhaustion.  Sometimes 
death  occurs  from  heart  failure  days  after  the  temperature  has 
become  normal  and  the  spasms  have  ceased.     The  symptoms,  in 


ORGANIC    WAR-LESIONS  531 

cases  of  recovery,  may  gradually  subside  in  a  week,  or  may  last 
as  long  as  a  couple  of  months.  Patients  who  survive  ten  days 
or  a  fortnight  from  the  original  onset  of  the  spasms,  generally 
recover. 

The  condition  has  to  be  distinguished  from  strychnine-poisoning. 
In  tetanus,  between  the  spasms  there  is  not  complete  relaxation 
of  the  affected  muscles  ;  they  remain  tonically  contracted,  unlike 
strychnine-poisoning,  in  which  there  are  complete  intermissions,- 
and  in  which  there  is  no  muscular  rigidity  between  the  spasms. 
Moreover,  in  strychnia-poisoning  the  fingers  and  hands  are  earliest 
affected,  not  the  jaws  or  face. 


WOUNDS  OF  THE  PERIPHERAL  NERVES 

War-lesions  of  the  peripheral  nerves  are  extremely  common. 
For  example.  Captain  Arthur  Evans  and  myseK  had  under  our 
personal  observation  exactly  300  cases  within  a  single  year.  Of 
these,  172  (or  57-3  per  cent.)  were  in  the  nerves  of  the  upper  Hmbs, 
inclusive  of  brachial  plexus  lesions  ;  81  (or  27  per  cent.)  in  the 
lower  limbs,  inclusive  of  cauda  equina  lesions ;  whilst  42  (or  14 
per  cent.)  were  cranial-nerve  palsies. 

The  lesions  produced  by  war  injuries  of  peripheral  nerves  are  of 
various  kinds. 

1.  The  nerve  may  be  completely  divided  by  a  missile  or  by 
a  bayonet  or  sword  wound.  In  such  cases  there  is  immediate  and 
complete  loss  of  function  of  the  nerve,  with  sensory  and  motor 
paralysis  in  the  area  of  distribution  of  the  fibres  below  the  level 
of  the  lesion.  The  paralysed  muscles  undergo  atrophy.  Trophic 
changes  may  also  develop  in  the  skin  and  nails  within  the  cutaneous 
distribution  of  the  nerve.  The  symptoms  remain  stationary,  and 
show  no  tendency  to  improve,  despite  assiduous  treatment. 

Sometimes  the  severed  ends  of  the  nerve  retract,  leaving  a  gap 
between  the  upper  and  lower  segments,  which  becomes  filled  up 
by  dense  scar-tissue.  In  the  course  of  a  few  weeks  a  bulbous 
swelling,  or  false  neuroma,  forms  on  the  stump  of  the  proximal 
segment  of  the  divided  nerve,  whilst  the  distal  segment  of  the 
nerve,  the  part  below  the  level  of  the  lesion,  becomes  thin  and 
wasted.  Partial  regeneration  of  nerve  fibres  may  subsequently 
occur  in  this  un-united  distal  segment,  but  regeneration  of  this 
sort  is  imperfect,  and,  so  long  as  the  nerve  fibres  of  the  proximal 


532 


NERVOUS    DISEASES 


segment  liave  not  been  united  by  operation,  it  remains  incomplete. 
Meanwhile  the  sensory,  motor,  and  trophic  phenomena  in  the 
paralysed  parts  remain  as  before. 

The  following  is  an  example  of  total  division  of  the  ulnar  nerve 
above  the  wrist  : — 

A  soldier,  aged  twenty-one,  when  disarming  a  party  of  German 
prisoners,  was  shot  by  one  of  them  at  point-blank  range,  sustaining 
a  large  lacerated  wound  in  the  lower  third  of  the  left  forearm  at 
its  ulnar  edge.  A  radiogram  showed  that  about  an  inch  of  the  ulna 
was  missing,  close  above  the  head  of  the  bone.  The  lowest  part  of 
the  ulna,  however,  together  with  the  wrist  joint,  remained  uninjured. 


Fig.  264. — -Complete  division  of/the  left  ulnar  nerve  above  the  wrist. 

Ever  since  the  injury,  the  patient  had  noticed  weakness  and  loss  of 
feeling  in  the  hand. 

AVhen  examined  six  months  later,  the  original  wound  of  the  fore- 
arm was  soundly  healed.  There  was  anaesthesia  of  one  and  a  half 
ulnar  fingers  and  of  the  corresponding  portion  of  the  hand,  front  and 
back.  The  area  of  cotton-wool  loss  was  slightly  more  extensive  than 
that  to  pin-pricks  or  to  deep  pressure.  Joint  sense  was  lost  in  the 
two  ulnar  fingers. 

The  hand  was  in  the  characteristic  claw-hand  position,  with  in- 
ability to  extend  the  inter-phalangeal  joints.  The  fingers  were  semi- 
flexed, most  markedly  the  two  ulnar  fingers,  whilst  there  was  slight 
hyper-extension  of  the  nietacarpo-phalangeal  joints  (see  Fig.  264). 
The  long  flexors  and  extensors  of  the  fingers,  however,  still  con- 
tracted voluntarily.  Abduction  and  opposition  of  the  thumb  were 
normal,  since  the  thenar  muscles,  innervated  by  the  median  nerve, 
were    unaffected.       The    interossei    and    hypothenar    muscles    were 


ORGANIC   WAR-LESIONS 


533 


wasted  and  paralysed,  so  that  spreading  out  the  fingers  was  juipossiijle 
(Fig.  264). 

There  was  a  small  trophic  blister  on  the  dorsum  of  the  little  finger, 
over  its  proximal  inter-phalangeal  joint.  The  hand  sweated  exces- 
sively on  the  palm,  except  in  the  ulnar  area,  which  remained  dry. 

2.  The  nerve  may  be  partially  divided.  In  such  cases  the 
symptoms  of  nerve  paralysis  are  partial,  corresponding  to  the 
particular  fibres  which  have  been  divided.  Here  also  a  neuroma 
forms  on  the  partially-divided  nerve,  at  the  side  corresponding 
to  the  severed  portion.  The  distal  fibres,  in  this  case,  being  attached 
laterally  by  connective  tissue  to  the  uninjured  part  of  the  nerve 
trunk,  cannot  retract.  The  histological  changes,  however,  con- 
sisting of  degeneration  follo^s'ed  by  regeneration,  are  the  same  as 
in  a  divided  nerve. 

In  cases  of  partial  division,  pain  is  a  comnion  symptom.  It 
is  referred  to  the  area  of  distribution  of  the  affected  nerve 
fibres,  and  is  sometimes  of  great  intensity.  Trophic  changes  in 
the  skin  and  nails  are  not  uncommon.  Hyperkeratosis,  or  exces- 
sive growth  of  epitheHum,  is  occasionally  a  marked  feature  (see 
Fig.  266).  In  some  cases  there  is  excessive 
sweating,  and  in  others  excessive  dryness,  of 
the  area  of  skin  supplied  by  the  partially- 
divided  nerve. 

The  following  is  an  example  of  partial 
division  of  the  median  nerve  in  the  lower 
part  of  the  forearm  : — 

A  sergeant-major,  aged  thirty-eight,  was 
wounded  in  the  right  forearm  at  a  range  of 
about  twenty  yards.  The  entry  wound  was  two 
and  a  half  inches  above  the  styloid  process  of 
the  radius,  the  exit  was  three  inches  above  the 
styloid  process  of  the  ulna,  both  wounds  being 
on  the  flexor  aspect  of  the  forearm.  The  bones 
were  not  fractured. 

Ever  since  the  injury,  the  patient  observed 
deficiency  of  sensation  on  the  front  and  back 
of  the  thumb,  index,  and  medius,  and  in  the 

corresponding  portion  of  the  palm.     He  also  had  difficulty  in  com- 
pletely flexing  the  index  and  medius. 

Four  weeks  after  the  injury  he  began  to  have  severe  pain  in  the 
thumb  and  thenar  region,  also  in  the  index  ;  the  pain  was  constant  and 
burning  in  character,  aggravated  by  moisture,  e.g.  on  washing  the 
hands. 

On  examination,  thirty  days  after  the  injury,  the  scars  of  the  entry 


Fig.  265.— Case  of  in- 
complete lesion  of 
the  median  nerve 
in  the  lower  part  of 
the  forearm. 


534 


NERVOUS   DISEASES 


and  exit  wounds  were  as  above  described.  Deep  pressure  in  the  fore- 
arm, midway  between  the  wounds,  caused  a  thrill  to  be  felt  in  the 
thumb,  index,  and  medius.  To  pin-pricks  and  cotton-wool  touches 
there  was  loss  of  sensation  on  the  palmar  aspect  in  the  thumb,  index, 
and  medius,  and  in  the  corresponding  portion  of  the  palm.  On  the 
dorsal  aspect  there  was  anaesthesia  of  the  same  three  digits  up  to 
the  metacarpo-phalangeal  joints  (see  Fig.  265).  Joint  sense  was  normal 
in  all  the  digits.  There  was  astereognosis  in  the  anaesthetic  fingers, 
as  tested  by  a  chain  and  a  coin  ;  with  the  two  ulnar  fingers  stereognosis 
was  perfect. 

Flexion  of  all  the  digits  was  possible,  but  distinctly  weaker  in  the 
index  and  medius  than  in  the  thumb,  ring,  or  little  finger.  The  thumb 
movements  could  be  freely  executed  in  all  directions,  although  the 
thenar  muscles  were  flabby.     The  interossei  were  normal. 

To  faradism  all  the  muscles  of  the  forearm  and  hand  reacted  briskly. 

As  an  example  of  hyperkeratosis  from  a  partial  nerve  lesion 
the  following  case  of  punctured  wound  of  the  ulnar  nerve  may 
be  taken  : — 

The  patient,  aged  twenty,  during  a  voyage  on  board  a  transport 
in  the  Mediterranean,  was  carrying  an  empty  soda-water  bottle  when 

the  ship  suddenly  gave  a  violent 
roll.  He  fell,  the  bottle  broke, 
and  a  fragment  of  glass  penetrated 
the  palm  of  the  left  hand  between 
the  thenar  eminence  and  the  pisi- 
form bone.  Ever  since  the  injury 
lie  had  been  unable  to  extend  the 
interphalangeal  joints  of  the  two 
ulnar  fingers,  and  noticed  deficient 
sensation  in  the  ulnar  area  of  the 
hand. 

When  examined  two  months 
later,  there  was  total  anaesthesia 
to  cotton-wool  and  pin-pricks  in 
the  front  of  one  and  a  half  ulnar 
fingers  and  the  corresponding  por- 
tion of  the  palm  (see  Fig.  266a). 
The  dorsum  was  anaesthetic  only 
over  the  fifth  metacarpal  bone  (the 
dorsal  cutaneous  branch  of  the 
nerve  having  been  given  off  above 
the  level  of  the  lesion).  Joint 
sense  was  lost  in  the  little 
finger. 


Fig.  266.  —  Hyiierkcralosis  of  palm 
from  partial  ulnar  nerve  lesion. 


There  was  slight  claw-hand,  the  two  ulnar  fingers  being  habitually 
semi- flexed  at  the  inter-phalangeal  joints  and  slightly  hyper-extended 
at  the  metacarpo-phalangeal  joints.  There  was  moderate  wasting  of 
all  the  interossei.     The  thumb  movements  were  normal.     He  could 


ORGANIC   WAR-LESIONS 


535 


feebly  spread  out  the  index  and  little  fingers,  but  not  the  middle  or  ring 
finger.  Extension  of  the  inter])halangeal  joints  of  the  fingers  was  im- 
possible. To  faradism  the  thenar  muscles  all  reacted  normally,  whereas 
there  was  no  reaction  in  the  interossei. 
There  was  marked  hyperkeratosis  of  the 
ulnar  side  of  the  palm  and  two  ulnar  fingers 
also  extending  slightly,  in  a  patchy  fashion, 
along  the  outer  side  of  the  palm  (see 
Fig.  266). 

3.  The  nerve   may   be   contused, 

without  being  anatomically  divided. 
Blood  is  extravasated  witliin  and  around 
the  unsevered  nerve  sheath,  compress- 
ing the  nerve  fibres  within.  In  severe 
contusion  the  nerve  fibres  undergo  degeneration,  just  as  if 
they  had  been  divided  by  a  cutting  or  lacerating  force.  Later, 
as  the  blood  becomes  absorbed,  a  dense  fibrous  scar  may  form 
within  and  around  the  nerve,  so  that  spontaneous  reunion  of  the 


Fig.  26Ga. — Area  of  anaesthesia 
in  the  case  of  ulnar  palsy 
shown  in  Fig.  266. 


Fig.  267. — Bullet  wound  of  musculo-spiral  nerve,  showing  entrance 
and  exit  wound,  together  with  the  resulting  drop- wrist.  (The 
dark  line  crossing  the  picture  above  the  level  of  the  wound  is 
the  shadow  of  a  vertical  bar  behind  the  patient.) 

nerve  is  sometimes  impossible.  In  less  severe  cases,  however, 
spontaneous  recovery  occurs  within  a  few  days  or  weeks,  without 
the  nerve  fibres  having  undergone  degeneration.  The  preserva- 
tion of  normal  electrical  reactions,  together  with  the  rapid  recovery 


536  NEKVOUS   DISEASES 

from  initial  anaesthesia,  are  indications  that  the  lesion  is  likely 
to  recover  spontaneously. 

The  following  is  an  illustrative  example  of  contusion  of  the 
musculo-spiral  nerve  : — 

The  patient,  aged  twenty-two,  was  wounded  by  a  bullet  which 
traversed  the  left  upper  arm,  entering  through  the  middle  of  the  tri- 
ceps and  emerging  at  the  outer  side  of  the  biceps  about  two  inches 
higher  up.  The  bullet  track  thus  crossed  the  limb  at  right  angles  to 
the  musculo-spiral  groove  (see  Fig.  267).  The  humerus  was  not  frac- 
tured. Drop-wrist  immediately  supervened,  together  with  a  subjective 
sensation  of  discomfort  referred  to  the  dorsum  of  the  hand  at  the 
radial  side. 

On  examination  seven  days  after  the  injury,  there  was  slight  com- 
parative blunting  to  cotton-wool  touches  and  pin-pricks  on  the  radial 
side  of  the  hand  and  fingers,  too  indefinite  to  be  charted.  Joint  sense 
was  normal  in  all  the  digits.  There  was  drop-wrist,  with  total  paralysis 
of  the  extensors  of  the  fingers,  wrist,  and  thumb,  also  of  the  supinator 
longus.  All  the  other  muscles  of  the  limb  contracted  normally.  To 
faradism  all  the  muscles  reacted  briskly,  including  the  paralysed  muscles. 

The  hand  was  placed  on  a  dorsiflexion-splint  and  within  a  week 
the  motor  paralysis  disappeared. 

The  next  case  is  a  still  slighter  examj)le  of  contusion  of  the 
musculo-spiral : — 

A  soldier,  aged  twenty-six,  was  wounded  by  a  small  fragment  of 
shell  which  entered  the  left  arm  an  inch  above,  and  half  an  inch  in 
front  of,  the  external  condyle.  There  was  no  wound  of  exit,  but  the 
metallic  fragment  could  be  felt  subcutaneously,  half  an  inch  higher 
up  the  limb,  internal  to  the  inner  edge  of  the  biceps. 

Immediately  after  he  was  wounded  the  wrist  dropped,  and  this 
wrist-drop  was  still  complete  when  he  came  under  observation  eight 
days  later.  Ever  since  the  injury  he  had  complained  of  a  constant 
subjective  pain  on  the  dorsal  aspect  of  the  metacarpo-phalangeal 
joint  of  the  index  finger,  spreading  round  the  web  of  the  thumb  to  the 
dorsum  of  the  terminal  phalanx  of  the  thumb.  This  pain  was  of  a 
scalding  character,  aggravated  by  light  touches  of  the  part,  and  also 
by  coughing  or  sneezing.  It  was  somewhat  relieved  by  warmth. 
Washing  in  cold'water  aggravated  the  pain. 

Five  weeks  after  the  injury,  no  cutaneous  anaesthesia  or  analgesia 
could  be  detected  on  careful  testing.  The  motor  paralysis  had  com- 
pletely cleared  up,  and  all  the  muscles  reacted  normally. 

The  following  is  a  good  example  of  contusion  of  the  popliteal 
nerves  and  vessels,  without  any  external  wound  whatever  : — 

A  gunner,  aged  twenty-seven,  when  standing  beside  his  gun,  was 
struck  at  the  back  of  the  right  knee  by  a  large,  smooth  fragment  of 
prematurely-exploded  shell  from  a  howitzer  battery  a  quarter  of  a 


ORGANIC   WAR-LESIONS 


537 


mile  to  Ills  rear.  No  cutaneous  wound,  or  abrasion  was  produced.  Ha  was 
knocked  down  by  the  blow,  and,  on  trying  to  get  up,  found  he  couhl 
not  stand.  The  right  leg  ininiediately  began  to  swell  from  the  knee 
downwards,  and  he  had  aching,  burning  pain  in  the  foot  and  leg. 

When  admitted  to  hospital,  eight  days  later,  there  was  much 
oedema  of  the  right  leg  and  foot.  Nevertheless  the  posterior  tibial 
artery  could  be  felt  pulsating  behind  the  internal  malleolus.  The 
oedema  lasted  for  nearly  four  weeks.  When 
it  subsided,  the  patient  found  himself  unable 
to  dorsiflex  the  right  ankle. 

On  examination,  five  weeks  after  the 
injury,  a  mass  of  deep-seated  induration 
could  be  felt  in  the  popliteal  space  behind 
the  head  of  the  right  fibula.  It  was  not 
pulsatile.  To  cotton-wool  touches  there 
was  anaesthesia  of  the  right  foot  and  leg, 
except  at  its  inner  side,  front,  and  back 
(see  Fig.  268).  Pressure  pain  was  not  felt  in 
the  ansesthetic  area.  To  pin-pricks  the  area 
of  loss  was  less  extensive  than  that  to  cotton- 
wool.    Joint  sense  was  normal. 

The  patient  could  invert,  evert,  and 
extend  the  ankle,  but  was  unable  to  dor- 
siflex the  ankle  or  make  any  voluntary 
movement  of  the  toes.  The  knee-jerks  and 
ankle-jerks  were  brisk  and  equal.  Both 
plantar  reflexes  were  present,  flexor  in  type, 
despite  the  apparent  paralysis  of  the  toes. 

To  faradism  there  was  no  reaction  in  the 
peronei,  tibialis  anticus,  or  extensors  of 
the  toes.  All  the  other  muscles  of  the 
leg  and  foot,  including  the  long  flexors  of  the  toes,  reacted  normally. 

Five  weeks  later,  anaesthesia  had  disappeared  from  the  territory  of 
the  internal  popliteal,  and  was  now  confined  to  the  dorsum  and  outer 
side  of  the  foot  and  leg.  Voluntary  flexion  of  the  toes  had  been 
recovered,  whilst  feeble  extension  of  the  toes  was  just  beginning. 

4.  The  nerve  may  be  "  concussed,"  i.e.  it  undergoes  a  sudden 
molecular  change  whereby  temporary  paralysis  occurs,  both  of 
its  sensory  and  motor  functions.  Nevertheless  its  nerve-fibres 
are  undivided,  and  within  a  short  time  complete  restitution  of 
function  sets  in,  sometimes  within  a  few  hours,  in  other  cases 
only  after  several  days. 

5.  The  nerve  may  undergo  gradual  compression,  e.g.  by  a 
tourniquet,  or  by  displaced  bony  fragments,  or  by  the  formation  of 
callus  around  a  healing  fracture.  In  such  cases  recovery  cannot 
be  expected  until  the  compression  is  relieved.  The  following 
is  an  illustrative  example  : — 


Fig.  268.— Aiisesihesia  in 
a  case  of  contusion  of 
the  popliteal  nerve  of 
the  right  lower  limb, 
without  any  external 
wound. 


538  NERVOUS   DISEASES 

A  soldier,  aged  thirty,  was  hit  in  the  region  of  the  right  shoulder 
by  a  bullet  which  entered  two  and  a  quarter  inches  below  the  tip  of 
the  acromion  process.  There  was  no  wound  of  exit,  but  a  metallic 
fragment  could  be  felt  under  the  skin  at  the  back  of  the  arm,  three 
inches  above  the  olecranon  process.  The  humerus  was  fractured  by 
the  bullet.  The  patient's  arm  dropped  powerless  at  the  moment  of 
injury,  and  the  wrist  is  said  to  have  dropped  at  the  same  time. 

When  examined,  two  and  a  half  months  later,  the  fracture  had 
become  firmly  united,  and  there  was  a  mass  of  callus  easily  felt  in  the 
region  of  the  musculo-spiral  groove.  To  pin-pricks  there  was  an  area 
of  analgesia  of  the  dorsum  of  the  hand  and  of  the  3|  radial  digits, 
except  on  their  terminal  phalanges.  Joint  sense  was  everywhere  normal. 
There  was  paralysis  and  loss  of  faradic  excitability  in  the  supinator 
longus,  and  the  extensors  of  the  wrist,  thumb,  and  fingers.  All  other 
muscles  of  the  arm,  forearm,  and  hand  were  normal. 

On  exposing  the  musculo-spiral  nerve  in  the  upper  arm,  it  was  found 
embedded  in  the  bony  callus  and  fibrous  tissue.  The  nerve  trunk  had 
not  been  divided.  At  one  point,  however,  there  was  a  well-marked 
stricture  of  fibrous  tissue,  strangling  the  nerve.  The  callus  was 
chiselled  away,  the  nerve  was  freed  from  its  bony  groove,  the  fibrous 
constriction  was  dissected  off,  and  a  small  portion  of  triceps  muscle 
was  fixed  between  the  nerve-trunk  and  the  bone,  to  prevent  future 
implication  by  fresh  bony  callus. 

6.  The  nerve  may  be  stretched  or  even  ruptured  by  a 

powerful  tearing  force,  applied  at  a  distance  from  the  actual 
point  which  gives  way.  This  sort  of  injury  may  result  from  a 
sudden  wrench,  as  when  a  soldier  is  hurled  against  a  stony  surface 
by  a  shell  explosion,  landing  on  the  top  of  his  shoulder  and 
lacerating  some  of  the  roots  of  the  brachial  plexus.  Less  fre- 
quently similar  laceration  of  nerve  fibres  may  occur  as  a  result  of 
sudden  muscular  exertion.    The  following  is  an  illustrative  case  : — 

A  soldier,  aged  twenty-five,  a  man  of  powerful  physique,  a 
blacksmith  in  civil  life,  was  engaged  one  day  in  pier-building  on 
the  Grallipoli  Peninsula,  when,  during  an  effort  to  raise  a  heavy  stone, 
he  felt  a  sudden  pain  above  the  right  scapula,  and  immediately  had 
difficulty  in  raising  the  right  upper  limb  above  the  head.  This  weak- 
ness increased  and  attained  its  maximum  within  a  couple  of  days. 
A  moderate  degree  of  pain  also  persisted  around  the  right  shoulder 
region. 

When  examined  a  month  later,  he  had  isolated  paralysis  of  the  right 
trapezius,  except  in  its  uppermost  (claviculo-acromial)  fibres  (which 
are  supplied  exclusively  by  the  spinal  accessory  proper).  The  middle 
and  lower  fibres  (innervated  by  the  3rd  and  4th  cervical  roots,  which 
help  to  form  the  sub-trapezial  plexus)  were  completely  paralysed  and 
inactive  to  faradism.  All  the  other  muscles  of  the  shoulder  girdle, 
and  the  serratus  magnus  in  particular,  contracted  normally  and  gave 


ORGANIC   WAR-LESIONS 


539 


brisk  responses  to  faradism.  There  was  an  area  of  analgesia  to  pin- 
pricks at  and  below  the  tip  of  the  right  shoulder,  corresponding  to  the 
distribution  of  the  4th  cervical  nerve. 

The  scapula  showed  the  typical  posture  of  trapezius  paralysis, 
being  displaced  outwards  and  downwards  en  masse,  and  also  rotated, 
so  that  its  lower  angle  was  tilted  inwards.  Together  with  this  there 
was  marked  winging  of  the  scapula  on  raising  the  arm  horizontally  in 
front  of  the  trunk  (see  Fig.  269).  At  the  beginning  of  this  movement, 
if  observed  from  the  front,  the  tip  of  the  right  scapula  could  be  seen 
displaced  upwards  by  the  unopposed  action  of  the  levator  anguli 
scapulae,  no  longer  antagonised  by  the  lower  fibres  of  the  trapezius. 


Fig.  2Gil. — Paralysis  of  third  and  fourtli  cervical  nerves  of  right  sub-trapezial 
plexus,  showing  winging  of  scapula  from  trapezius  palsy.  The  area  of 
sensory  loss  at  the  tip  of  the  shoulder  is  also  indicated. 

In  this  case  the  lesion  is  obviously  one  of  the  sub-trapezial  plexus, 
of  which  the  3rd  and  4th  cervical  nerves  have  become  completely 
paralysed,  whilst  the  spinal  accessory  proper,  or  at  least  those  of  its 
fibres  which  innervate  the  uppermost  fibres  of  the  trapezius,  have 
escaped. 

7.  The  nerve  may  become  inflamed.  This  form  of  neuritis  is 
often  due  to  septic  infection  of  the  wound.  It  may  also  occur, 
however,  without  obvious  signs  of  infection.  A  complication  of 
this  sort  retards  all  the  processes  of  repair  or  regeneration,  no  matter 
how  mild  the  infection  may  be.  In  such  cases  of  neuritis,  in  addi- 
tion to  the  signs  of  a  nerve  lesion,  whether  complete  or  incomplete, 
pain  is  a  specially  prominent  feature.  The  pain  of  traumatic 
neuritis  is  usually  intense.  It  is  referred  to  the  sensory  distribution 
of  the  nerve,  and  is  accompanied  by  marked  cutaneous  hyper- 


540  NERVOUS    DISEASES 

aesthesia  and  by  tenderness  along  the  course  of  tlie  nerve  trunk 
at  and  below  tbe  site  of  injury.  Tbe  pain  is  of  a  burning  cbaracter, 
aggravated  by  dryness  and  heat,  by  light  cutaneous  stimuli,  and 
even  by  sneezing  or  coughing,  or  by  any  other  sudden  movement 
of  the  body.  It  is  somewhat  relieved  by  cold  and  moist  appli- 
cations, and  the  patient  tends  spontaneously  to  keep  his  affected 
hand  or  foot  swathed  in  moist  bandages.  Painful  neuritis  of  this 
sort  is  specially  common  in  the  median  and  sciatic  nerves.  The 
pain  of  a  traumatic  neuritis  sets  in  some  ten  days  or  a  fortnight 
after  the  original  wound.  It  gradually  increases  in  intensity,  and 
for  several  weeks  remains  at  its  maximum.  Then  it  slowly  dimin- 
ishes and  spontaneously  disappears  in  the  course  of  months.  The 
natural  history  of  these  cases  is  important  to  bear  in  mind,  since 
surgical  intervention  is  unavailing,  and  relief  must  be  sought  from 
electrical,  physical,  or  medicinal  remedies. 

Clinically,  these  various  classes  of  nerve  lesions  are  not  always 
clearly  marked  off,  one  from  the  other.  Although  it  is  usually 
easy  to  say  that  a  particular  nerve  has  not  been  damaged,  it  is 
sometimes  difficult,  in  the  case  of  a  paralysed  nerve,  to  decide 
whether  the  lesion  is  an  actual  severance  or  only  a  contusion. 
Each  case  must  be  considered  on  its  own  merits. 

In  every  case  of  motor  paralysis  from  a  peripheral  nerve  lesion, 
the  electrical  reactions  (at  a  date  not  sooner  than  ten  days  after 
the  original  injury)  should  be  carefully  observed.  The  presence  or 
absence  of  K.D.  will  have  important  significance,  both  in  diagnosis 
and  in  prognosis.  It  is  worth  remembering  that  we  may  sometimes 
have  electrical  changes  in  muscles  which  are  functionally  active. 
In  paralysed  muscles  which  have  lost  their  faradic  response  volun- 
tary power  usually  reappears  earlier  than  faradic  excitability. 

Cranial-nerve  Injuries. — Notwithstanding  the  great  frequency 
of  head  wounds,  especially  in  trench  warfare,  it  will  be  observed 
that  cranial-nerve  palsies  are  relatively  less  common  than  injuries 
of  the  spinal  nerves.  For  each  case  of  cranial-nerve  paralysis  we 
meet  with  two  cases  of  lesion  of  the  nerves  of  the  lower  limbs  and 
four  cases  of  injury  to  the  brachial  plexus  and  its  branches.  This 
is  easily  understood.  Most  wounds  which  traverse  the  base  of  the 
skull  are  fatal,  and  only  a  small  proportion  of  such  patients  sur- 
vive to  show  cranial-nerve  paralysis.  In  those  which  do  survive, 
the  lesion  is  almost  always  extra-cranial,  e.g.  from  wounds  of  the 
orbit,  face,  mastoid  region,  or  upper  part  of  the  neck. 


ORGANIC   WAR-LESIONS 


541 


The  cranial  nei-ve  most  frequently  injured  is  the  facial.  Next 
in  frequency,  as  seats  of  single  nerve  lesions,  come  the  trigeminal 
nerve  and  the  spinal  accessory.  But  it  is  a  common  occurrence  for 
more  than  one  nerve  to  be  implicated  in  the  same  wound. 

The  symptomatology  of  individual  cranial-nerve  palsies  is 
famiUar,  and  has  already  been  discussed  in  Chapters  IX  and  X. 
It  may  be  useful,  however,  to  mention  a  few  illustrative  examples 
of  multiple  cranial-nerve  injuries. 

Bullet  wound  of  orbit,    with  paralysis  of  ocular  nerves  and 

cavernous  sinus  syndrouie  : — 

A  soldier,  aged  twenty,  was  wounded  by  a  rifle  bullet  which  entered 
the  right  side  of  the  face  half  an  inch  below  and  internal  to  the  malar 


Figs.  270a  and  270b. — Kadiograms  showing  bullet  in  outer  wall  of  left  orbit, 
producing  ocular  paralysis,  proptosis,  and  chemosis. 

eminence.  There  was  no  wound  of  exit.  The  patient  felt  nothing 
wrong  until  two  days  later,  when  the  left  eyelids  swelled  up  {i.e.  on 
the  opposite  side  irova  the  entry  wound),  so  that  he  could  no  longer  see 
with  that  eye. 

When  examined  nine  days  after  the  injury,  there  was  still  marked 
oedema  of  the  left  upper  lid,  together  with  chemosis  of  the  left  con- 
junctiva and  some  sub-conjunctival  hsemorrhage.  The  left  eye  was 
markedly  proptosed,  and  its  movements  upwards,  outwards,  and  in- 
wards were  restricted.  Downward  movement  was  good.  There  was 
diplopia  in  all  positions  of  the  eyes.  The  optic  discs  were  normal. 
The  pupils  were  equal  and  normal.  The  right  eye  was  normal  in  all 
respects. 

Radiograms  (Figs.  270a  and  270b)  showed  a  bullet  in  the  posterior 
part  of  the  left  orbit,  towards  its  outer  wall.  It  was  subsequently 
successfully  extracted  through  an  incision  in  the  temporal  fossa,  after 
removal  of  the  outer  wall  of  tlie  orbit. 


542  NERVOUS   DISEASES 

Combined  lesion  of  trigeminal  and  facial : — 

Fig.  271  shows  a  trooper  who  was  struck  by  a  fragment  o±  snell, 
which  entered  behind  the  right  pinna,  immediately  in  front  of  the 
tip  of  the  mastoid  process,  emerging  close  behind  the  right  ala  nasi. 

When  examined  eight  days  after  the  injury,  there  was  some  ecchy- 
mosis  under  the  right  conjunctiva,  below  and  to  the  outer  side  of  the 
iris.     There  was  an  area  of  anaesthesia  to  cotton-wool  touches  and  pin- 


FiG.  271. — Wound  of  right  upper  facial  nerve  and  of  right 
infra-orbital  nerve.  The  arrovsr  indicates  the  direction 
of  the  entry  wound.  The  patient  is  looking  upwards  to 
display  a  subconjunctival  hsemorrhage  in  the  right  eye. 

pricks  on  the  right  cheek,  and  part  of  the  right  upper  lip.  There  was 
no  anaesthesia  of  the  roof  of  the  mouth,  upper  gum,  or  inner  surface 
of  lip.  The  masseters  and  temporals  were  powerful  on  both  sides. 
The  right  facial  muscles  were  distinctly  weaker  than  the  left,  especially 
the  frontalis  muscle.  This  weakness  was  well  seen  when  the  patient 
looked  upwards  and  wrinkled  the  forehead.  The  lower  facial  muscles 
were  but  slightly  affected.  All  the  other  cranial  nerves  were  normal. 
To  faradism  there  was  slight  diminution  of  excitability  in  the  right 
facial  muscles. 

The  next  case  is  one  of  combined  lesion  of  the  facial  and  of  the 
palatal  branch  of  the  vagus  : — 

This  patient,  aged  nineteen,  was  wounded  by  a  shrapnel  bullet 
which   entered  through  the   tip   of  the  right  mastoid  process.     He 


ORGANIC   WAR-LESIONS 


543 


states  that  the  bullet  rolled  out  of  his  mouth.     He  did  not  become  un- 
conscious.    His  face  at  once  became  twisted  (see  Fig.  272). 

When  examined  nine  days  after  the  injury,  there  was  total  right- 
sided  facial  paralysis,  upper  and  lower,  with  complete  loss  of  faradic 
excitability  in  the  afiEected  muscles.  Taste  was  unaffected.  Hearing 
was  also  intact,  both  to  aerial  and  bony  conduction.  On  phonation 
the  palate  was  pulled  upwards  and  to  the  left,  and  a  shallow  exit 
wound  was  seen  just  to  the  left  side  of  the  base  of  the  uvula.  The 
right  pinna  projected  abnormally  from  the  side  of  the  head,  owing  to 
swelling  of  the  tissues  around  the  wound  of  entrance. 


Fig.  272. — Eight-sided  facial  palsy  from  a  bullet  wound  enteriDg 
through  the  right  temporal  bone  and  emerging  through  the 
mouth.     The  right  side  of  the  palate  was  also  paralysed. 

The  following  case  is  one  of  hypoglossal  and  cervical  sympa- 
thetic paralysis,  with  transient  paresis  of  the  facial : — 

A  soldier,  aged  twenty-three,  was  wounded  at  Suvla  by  a  bullet 
which  entered  through  the  left  parotid  region,  an  inch  above  and  in 
front  of  the  angle  of  the  jaw.  There  was  no  exit  wound,  but  the 
bullet  track  evidently  passed  downwards  and  inwards. 

When  examined  ten  days  later,  there  was  paralysis  of  the  left 
side  of  the  tongue,  which,  when  protruded,  deviated  markedly  to  the 
left  in  a  characteristic  sickle-shaped  fashion.  There  was  also  weakness 
of  the  left  face,  complete  in  the  lower,  partial  in  the  upper  muscles. 
To  faradism  there  was  loss  of  reaction  in  the  whole  of  the  left  facial 
muscles  and  in  the  left  half  of  the  tongue.  The  parotid  gland  in  the 
region  of  the  entry  wound  was  swollen.  The  facial  weakness  rapidly 
cleared  up,  but  the  hypoglossal  paralysis  persisted,  and  in  a  few  days 
it  became  evident  that  the  cervical  sympathetic  had  been  damaged, 
as  evidenced  by  the  presence  of  pseudp-ptosis,  enophthalmos,  nar- 
rowing of  the  palpebral  fissure,  and  contraction  of  the  left  pupil  (see 
Fig.  273).  The  parotid  swelling  still  persisted,  and  it  was  possible  to 
express  saliva  through  the  wound. 


544 


NERVOUS   DISEASES 


Injuries  of  the  Brachial  Plexus  and  of  its  Branches. — More 
than  haH  of  all  the  cases  of  peripheral  nerve  injuries  in  war  belong 
to  this  group. 

The  brachial  plexus  is  constituted  by  the  anterior  primary 
divisions  of  the  four  lowest  cervical  roots  (the  5th,  6th,  7th,  and 
8th),  together  with  the  1st  thoracic  root  (see  Fig.  274).  It  is 
unnecessary  here  to  recapitulate  the  anatomy  of  the  plexus,  the 
details  of  which  should  be  familiar  to  every  student  of  neurology. 


Fig.  273. — Wound  of  left  parotid  region,  with  paralysis 
of  left  hypoglossal  and  cervical  sympathetic. 

From  the  cUnical  standpoint,  it  is  convenient  to  consider 
brachial  plexus  injuries  in  three  classes  : — 

1.  Lesions  above  the  clavicle,  affecting  the  nerve- tiiinks  (upper, 
middle,  or  lower),  or  the  nerve-roots  from  which  these  nerve-tranks 
are  derived.  In  this  class  of  case  the  signs  and  symptoms,  both 
motor  and  sensory,  tend  to  be  distributed  in  a  radicular  fashion. 

2.  Lesions  lower  down,  in  the  region  of  the  axillary  vessels, 
where  the  cords  of  the  brachial  plexus  (inner,  outer,  and  posterior) 
surround  the  axillary  artery.  In  such  cases  the  wound  of  the  plexus 
commonly  damages  the  great  vessels  at  the  same  time. 

3.  Lesions  of  the  individual  nerves  of  the  linib,  after  they  have 


ORGANIC   WAR-LESIONS 


545 


left  the  plexus.  Some  of  these  nerves  [e.g.  the  median,  ulnar,  and 
internal  cutaneous)  accompany  the  brachial  artery  for  part  of  its 
course  ;  others  {e.g.  the  musculo-spiral  and  circumflex)  diverge 
from  the  main  vessels,  and  are  therefore  less  likely  to  be  compli- 
cated by  the  occurrence  of  traumatic  aneurisms  of  various  kinds. 

Complete  plexus  paralysis  is  rare  ;    partial  plexus  lesions  are 
common.     The  following  is  an  example  of  a  wound  in  which  the 


PERIPHERAL    NERVt   DISTRIBUTION 


ROOT  AREA  DISTRIBUTION. 


Rhomboids 

Spinal! 

Dekoid 

Biceps 

Broch  Anticus 

Supinators 

Pect  Major 
(Clavitr  portion.) 
Serrafus  Magnus 
Rod  Eit>  of  Wnst 
Pronators 
Pect  Major 
Triceps  I 

ExtCflrp.Ulnans  ( 
£xt»  of  Fingers   J 

Flexors  of  Wrist 
and  Fingers 
Intrinsic  Miucfes  V 
of  Hand  / 


POST?  THORACIC 
(Scmatus  Magnus) 


AWTTHORAaC      „ 
(Pectorals)     J^^ 

SUBSCAPUl^Ut 

(Subscopuloris 
Lohsslmus  Oorsi 
Ter«s  Major 


[Biceps 
MUSCULO-CUTANEOUS  <  Coroco-Bnochiolis 
~        [Brochialis  Anticus 

[Rad  Flexor  of  Wnst 
MEDIAN      J  Long  flexors  of  Fingers  4  ThumD 
IPronotors 
[Opponers  &  AWuctor  PoJIias 

ORCUMnXX  (Oeltoid 
(.Teres  Minor 

MUSCULO-      [Triceps 
rrjr-       J  Supinators 
M.^..n  ^^^^      Ext. Carpi  Rad 

ytME  [Exf  of  Fingers  4  Thumb 

Ulnar  Flexor  of  Wrist 


Lesser  Int. Cutaneous 


^      I  Ulnar  half  of  Flex.ProFbndus 
<>•      )  Hypothenar  Muscles 
Internal  and  U'lte^ossef «  Adductor  Pojlicis 


Fig.  274. — Diagram  of  brachial  plexus, 

whole  brachial  plexus  was  paralysed,  except  its  oculo-pupillary 
fibres  : — 


A  soldier,  aged  twenty,  was  wounded  by  a  bullet  which  entered 
immediately  above  the  left  clavicle,  three  and  a  half  inches  from  the 
middle  line.  There  was  no  exit  wound.  A  radiogram  showed  the 
bullet  lying  in  the  left  supra-spinous  fossa.  Immediately  on  being  hit, 
the  patient  lost  power  in  the  left  upper  limb. 

When  examined  two  weeks  after  the  injury,  no  pulsation  could  be 
detected  in  the  axillary,  brachial,  or  radial  artery  on  the  left  side  ; 
nevertheless  both  hands  were  equally  warm.  To  cotton-wool  and  pin- 
pricks there  was  anaesthesia  of  the  whole  of  the  upper  limb,  save  for  a 
small  strip  along  the  inner  side  of  the  upper  arm,  corresponding  to  the 
area  innervated  by  the  2nd  thoracic  root  (see  Fig.  275).  Passive  ab- 
duction of  the  shoulder-joint  caused  pain  ;  all  other  passive  movements 

2  M 


546 


NERVOUS    DISEASES 


were  unperceived.  Joint-sense  and  vibration-sense  were  lost  at  all 
parts  of  the  limb,  from  the  shoulder  downwards.  The  limb  was  flaccid 
and  paralysed  at  all  joints.  The  pectorals,  spinati,  latissimus,  and  all 
the  muscles  of  the  upper  arm,  forearm,  and  hand  were  completely- 
paralysed,  and  gave  no  reaction  to  the  faradic  battery.  The  pupils 
and  ocular  fissures,  however,  were  equal. 


Supra-clavicular  woulcI  of  left  brachial  plexus. 

Supra-clavicular  lesion  of  plexus,  affecting  5th  cervical  root  : — 

A  soldier,  aged  twenty-two,  sustained  multiple  shrapnel  wounds 
of  the  head,  right  shoulder,  and  right  knee.  Of  the  fragments,  one 
entered  half  an  inch  to  the  right  of  the  7th  cervical  spine  and  emerged 
through  the  outer  pectoral  region,  two  and  three-quarter  inches  below 
the  right  clavicle.  The  right  upper  limb  immediately  became  weak 
at  the  shoulder  and  elbow. 

On  examination  ten  days  after  the  injury,  there  was  anaesthesia 
to  pin-pricks  and  cotton-wool  on  the  outer  aspect  of  the  upper  limb, 
in  two  areas  corresponding  to  part  of  the  territory  of  the  5th  cervical 
nerve  (see  Fig.  276).  All  the  muscles  of  the  upper  limb  were  powerful, 
with  the  exception  of  the  deltoid,  biceps,  and  supinator  longus,  which 
were  totally  paralysed.  Nevertheless  the  elbow  could  still  be  feebly 
flexed  by  means  of  the  extensor  carpi  radialis  longior.  The  patient 
accomplished  this  by  previously  strongly  pronating  and  deviating  the 
wrist  to  the  ulnar  side,  so  as  to  give  the  muscle  an  advantage.  To 
faradism  there  was  loss  of  reaction  in  the  deltoid  and  supinator  longus, 
whilst  the  biceps  reacted  feebly.  All  the  other  muscles  of  the  limb 
reacted  briskly. 

A  week  later  the  biceps  had  recovered,  and  there  was  now  some 
voluntary  contraction  in  the  supinator  longus.  The  deltoid,  however, 
was  still  paralysed  and  the  anaesthesia  was  as  before. 


ORGANIC   WAR-LESIONS 


547 


Supra-clavicular  lesion  of  plexus,   affecting  8tli  cervical  and 
1st  thoracic  roots  : — 

An  Australian  soldier,  aged  twenty-five,  was  wounded  by  a  bullet 


Fig.  276. — Supra-clavicular  bullet  wound  of  brachial  plexus, 
implicating  5th  cervical  root. 

which  entered  posteriorly,  half  an  inch  to  the  right  side  of  the  middle 
line,  immediately  below  the  tip  of  the  7th  cervical  spine,  and  emerged 
through  the  middle  of  the  left  sterno-mastoid  muscle. 


Fig.  277. 


-Supra-clavicular  bullet  wound  of  left  brachial  plexus,  implicating 
8th  cervical  and  1st  thoracic  roots. 


When  examined  ten  days  after  the  injury,  there  was  an  area  of 
total  anaesthesia  to  all  forms  of  cutaneous  stimulation  along  the  inner 
side  of  the  left  forearm  and  hand,  including  1^  fingers  on  the  palmar 


548 


NERVOUS   DISEASES 


aspect  and  2^  fingers  on  the  doxsum  (see  Fig.  277).  All  movements  of 
the  scapula,  shoulder,  elbow,  and  wrist  were  normal.  The  thumb  was 
totally  paralysed,  also  all  the  intrinsic  hand  muscles.  Flexion  of  the 
fingers  was  impossible,  and  extension  was  impaired,  since  only  the  long 
•extensors  came  into  action,  unassisted  by  the  interossei.  To  faradism 
there  was  no  response  in  the  long  flexors  of  the  thumb  or  fingers,  nor 
in  the  thenar,  hypothenar,  or  lumbrical  muscles,  whilst  all  the  other 
muscles  of  the  forearm,  upper  arm,  and  shoulder  girdle  reacted  nor- 
mally. There  was  no  difference  between  the  pupils  or  ocular  fissures 
of  the  two  sides. 

The  following  is  an  example  of  a  brachial  plexus  lesion  in  which 
the  axillary  artery  was  wounded  as  well.  The  damage  to  the  plexus 
implicated  chiefly  its  posterior  and  inner  cords.     Owing  to  the 


Fig.  278. — Wound  of  left  brachial  plexus  and  of  axillary  artery. 

development  of  an  axillary  aneurism,  ligation  of  the  axillary  artery 
was  subsequently  performed.  This  was  followed  by  a  slight  increase 
in  the  extent  of  the  motor  paralysis,  together  with  loss  of  faradic 
excitability  in  nearly  all  the  muscles  of  the  limb — a  condition 
apparently  due  to  ischeemic  interstitial  myositis  (see  later,  p.  556). 

The  patient,  aged  twenty-eight,  was  wounded  by  a  bullet  which 
entered  through  the  anterior  part  of  the  left  deltoid  and  emerged  four 
inches  to  the  right  side  of  the  8th  thoracic  spine,  traversing  the  left 
lung  en  route.  The  left  upper  limb  at  once  fell  powerless  to  the  side. 
When  admitted  to  hospital  in  Malta,  five  days  later,  there  was  severe 
dyspnoea  owing  to  a  left-sided  hsemothorax  from  which  30  ounces  of 
dark  fluid  blood  were  removed  by  aspiration. 

Twelve  days  after  the  injury  the  dyspnoea  had  cleared  up,  and  it 
was  now  possible  to  examine  the  left  upper  limb.  This  showed  wide- 
spread anaesthesia,  chiefly  on  its  extensor  aspect,  but  also  in  the  ulnar 
distribution  of  the  hand  (see  Fig    278).     Joint  sense  was  lost  in  the 


ORGANIC   WAR-LESIONS  549 

little  finger  ;  all  other  joints  were  normally  sensitive.  There  was 
paralysis  of  the  deltoid  and  triceps.  The  biceps  was  strong,  and  the 
latissinius  dorsi  contracted  well  on  coughing.  There  was  paralysis 
of  the  supinator  longus,  also  of  the  extensors  of  the  wrist,  thumb, 
and  fingers.  The  long  flexors  of  the  wrist,  fingers,  and  thumb  were 
feeble,  but  not  completely  paralysed.  All  the  intrinsic  muscles  of  the 
hand  were  paralysed.  To  faradism  there  was  loss  of  reaction  in  the 
paralysed  deltoid,  triceps,  supinator  longus,  and  extensors  of  the  wrist, 
thumb,  and  fingers,  whilst  the  paralysed  thenar,  hypothenar,  and 
interosseal  muscles  all  reacted  briskly,  as  did  also  the  other  non- 
paralysed  muscles  of  the  limb. 

Fifteen  days  after  the  injury,  the  patient  began  to  complain  of  aching 
pain  in  the  limb,  from  the  shoulder  to  the  fingers,  and  on  the  nineteenth 
day  a  diffuse,  tender  swelling  was  found  in  the  upper  part  of  the  left 
axilla,  in  front  of  the  shoulder-joint.  A  pulsatile  bruit  was  to  be  heard 
over  this  swelling.  Both  radial  pulses,  however,  were  easily  felt,  and 
there  was  little  difference  in  the  blood-pressure  in  the  two  brachial 
arteries,  the  measurement  on  the  left  side  being  130/86  as  compared 
with  138/86  upon  the  healthy  side. 

On  the  twenty-first  day  the  axillary  artery  was  exposed  by  Captain 
Camps,  and  an  aneurism  was  found  to  occupy  the  third  part  of  the 
axillary  artery.  There  was  an  abnormally  high  bifurcation  of  the 
artery  above  the  aneurism,  which  might  perhaps  account  for  the 
practically  normal  pulse  below  the  aneurism.  The  vessel  was  liga- 
tured above  and  below  the  aneurism  and  the  clot  turned  out.  The 
wound  was  septic,  but  with  suitable  drainage  the  patient  made  a 
steady  recovery  from  the  operation. 

Eight  weeks  after  the  operation,  the  area  of  cutaneous  anaesthesia 
was  found  to  be  unchanged,  and  there  was  loss  of  joint  sense  in  the 
little  finger  as  before.  There  was  now  paralysis  of  the  biceps  and 
latissimus  dorsi,  which  prior  to  the  operation  had  contracted  briskly. 
The  paralysis  of  the  deltoid,  triceps,  extensors  of  the  wrist,  fingers, 
and  thunil3,  and  of  the  intrinsic  muscles  of  the  hand,  was  complete  as 
before,  and  there  was  well-marked  wasting  of  the  interossei.  He  could 
still  flex  the  fingers  and  thumb.  There  was  a  curious  change  in  the 
electrical  faradic  reactions.  There  was  now  no  reaction  in  any  muscle 
of  the  upper  limb,  from  the  pectoral  downwards,  except  a  feeble 
response  in  the  interossei  and  thenar  muscles  and  in  the  long  flexors 
of  the  fingers.  All  the  paralysed  muscles  of  the  upper  arm  and  forearm 
were  harder  and  tougher  in  consistence  than  normal,  suggesting  a 
condition  of  ischsemic  palsy.  The  pectoral  muscles,  although  not 
reacting  to  faradism,  contracted  well  voluntarily.  Both  radial  pulses 
could  be  felt  equally  well.  The  blood-pressure  in  the  left  brachial 
artery  measured  124/84,  as  compared  with  128/80  on  the  right^'side. 

The  next  case  is  one  in  which  the  brachial  plexus  lesion  was 
mainly  of  the  outer  cord  : — 

The  patient,  an  Australian  sapper,  aged  twenty-eight,  was  wounded 
by  a  bullet  which  entered  half  an  inch  below  the  right  clavicle,  just 
internal  to  the  coracoid  process.    The  exit  wound  was  large  and 


550 


NERVOUS   DISEASES 


oblique,  four  inches  long,  in  the  left  supra-spinous  fossa,  its  upper 
end  being  an  inch  to  the  left  of  the  4th  thoracic  spine.     The  patient, 


Fig.  279. — Bullet  wound  of  right  brachial  plexus. 

when  hit,  felt  his  arm  drop  powerless  at  once,  with  the  sensation  as  if 
he  had  received  a  blow  on  the  back.     There  was  no  hsemoptysis.     Within 

a  day  or  two  he  found  he 
could  move  his  shoulder, 
but  the  hand  remained  weak 
and  the  whole  limb  remained 
numb. 

When  examined  ten  days 
after  the  injury,  there  was 
widespread  anaesthesia  and 
analgesia  from  the  shoulder 
downwards,  with  the  excep- 
tion of  the  inner  side  of  the 
upper  arm  and  forearm  and 
the  median  and  radial  terri- 
tories of  the  hand  (see  Fig. 
279).  Joint-sense  was  lost  in 
all  the  digits  except  the 
thumb  ;  normal  at  the  wrist, 
elbow,  and  shoulder.  All 
the  scapular  and  shoulder 
muscles  were  powerful,  also 
the  triceps  and  extensors  of 
the  wrist,  fingers,  and  thumb. 
The  biceps  was  completely 
paralysed,  but  the  elbow 
could  still  be  fully  flexed  by  the  unparalysed  supinator  longus  (see 
Fig.  280).    The  pronators  were  paralysed.    The  supinators  were  normal. 


Fig.  280.— Bullet  wound  of  right  brachial 
plexus.  Although  the  biceps  is  para- 
lysed, the  patient  can  still  flex  the  right 
elbow  by  means  of  the  supinator  longus. 


ORGANIC   WAR-LESIONS 


.    551 


The  long  flexors  of  the  wrist,  thumb,  and  fingers  were  paralysed, 
together  with  all  the  intrinsic  muscles  of  the  hand.  The  hand  was 
habitually  flexed  at  the  two  ulnar  fingers,  and  lightly  flexed  at  the 
medius  and  index.  To  faradism  there  was  loss  of  reaction  in  the 
intrinsic  hand  muscles,  also  in  the  long  flexors  of  the  fingers,  thumb, 
and  wrist,  and  in  the  pronators.  The  biceps  reacted  feebly  ;  the 
extensors  of  the  wrist  and  fingers,  together  with  the  triceps,  deltoid,  &c., 
all  reacted  briskly. 

Injuries  of  the  Cauda  Equina. — The  chief  points  of  clinical 
importance  in  the  diagnosis  of  lesions  of  the  cauda  equina  and 
conns  medullaris  have  already  been  referred  to  (see  pp.  2-45-247 
and  Figs.  107  and  108),  and  it  is  unnecessary  here  to  recapitulate 
them.  It  may,  however,  be  useful  to  add  one  or  two  illustrative 
examples  of  partial  lesions,  in  which  the  damage  was  Hmited  to  a 
few  roots  of  the  cauda.  War-lesions  of  the  cauda  are  generally 
asymmetrical. 

The  following  case  is  one  in  which  the  lesion  was  confined  to 
the  left  half  of  the  cauda  equina,  from  the  5th  lumbar  root  down- 
wards : — 

The  patient,  an  Australian  gunner,  aged  twenty-five,  was  wounded 
by  a  rifle  bullet  which  entered  half  an  inch  to  the  left  of  the  4th  lumbar 
spine.  There  was  no  exit  wound, 
but  a  radiogram  showed  the  bullet 
lying  point  downwards  to  the 
right  of  the  middle  line  between 
the  bodies  of  the  11th  and  12th 
thoracic  vertebrae. 

When  he  was  struck,  his  legs 
gave  way,  he  "stiffened  out "  with 
transient  extensor  spasm,  and  was 
unable  to  stand  or  walk.  The 
right  lower  limb  was  never  para- 
lysed, but  the  left  limb  was  totally 
powerless  at  the  start,  and  he  also 
noticed  it  to  be  deficient  in  sensa- 
tion. Within  three  days  motor 
power  began  to  reappear  in  the 
left  toes.  There  was  some  delay 
in  micturition  at  first,  but  a 
catheter  was  never  required. 

AVhen  examined  ten  days  after 
the  injury,  there  was  loss  of  sensa- 
tion to  pin-pricks,  and  to  cold  and  heat,  in  the  left  lower  limb,  including 
nearly  all  of  its  posterior  aspect,  the  dorsum  of  the  foot  and  outer  side 
of  the  leg,  also  the  left  side  of  the  genitals.  The  inner  side  of  the  calf 
escaped,  together  with  part  of  the  sole  of  the  foot.     Joint -sense  was 


Fig.    281 


Unilateral  lesion  of  cauda 
equina,  with  anaesthesia  from  level 
of  5th  root  downwards,  on  the  left 
side. 


552  NEKVOUS   DISEASES 

lost  at  the  left  toes  and  ankle,  normal  at  the  knee  and  hip.  Cotton- 
wool touches  could  be  felt  all  over  the  analgesic  area.     (See  Fig.  281.) 

The  sensory  and  motor  functions  of  the  right  lower  limb  were 
normal. 

There  was  marked  weakness  of  the  left  lower  limb  in  the  quadriceps 
extensor  and  in  the  other  anterior  thigh  muscles,  also  in  the  calf  muscles, 
peronei,  and  anterior  tibial  group.  The  gluteal  and  adductor  muscles 
were  strong,  also  the  hamstrings. 

To  faradism  there  was  no  reaction  in  the  tibialis  anticus  nor  peronei, 
the  extensors  of  the  toes  reacted  feebly,  whilst  all  the  other  muscles 
of  the  limb  gave  a  brisk  reaction. 

The  left  ankle-jerk  was  absent,  the  right  was  brisk.  Both  knee- 
jerks  were  diminished,  especially  on  the  left  side.  The  bulbo-caver- 
nosus  reflex  was  brisk  ;  the  plantars  were  both  absent  ;  the  abdominal 
reflexes  were  present,  somewhat  brisker  on  the  right  side  than  on  the 
left. 

Within  a  week  further  improvement  had  occurred,  so  that  no 
individual  muscles  were  now  paralysed,  though  the  peronei  were 
relatively  feebler  than  the  rest,  and  the  patient  was  still  unable  to 
raise  the  extended  limb  off  the  bed  against  gravity. 

The  next  case  illustrates  a  bilateral  lesion  of  the  upper  part 
of  the  Cauda  equina,  affecting  on  the  right  side  the  roots  from  the 
2nd  lumbar  to  the  1st  sacral  inclusive,  and  on  the  left  side,  less 
severely,  the  5th  lumbar  and  1st  sacral  roots  : — 

An  officer  in  a  Highland  regiment,  aged  thirty-two,  was  taking  part 
in  a  gallant  attack  on  a  position,  advancing  by  a  succession  of  rapid 
rushes.  When  lying  down  between  two  of  these  rushes,  he  was  shot 
in  the  trunk,  the  bullet  entering  through  the  8th  intercostal  space 
on  the  right  side,  behind  the  posterior  axillary  fold.  There  was  no 
exit  wound,  but  a  radiogram  subsequently  showed  the  rifle  bullet  to 
be  lodged  in  the  left  hip  joint,  with  its  point  directed  upwards. 

When  shot,  he  had  a  sensation  as  if  the  feet  were  curling  up.  He 
lost  power  at  once  in  the  right  lower  limb,  i.e.  on  the  opposite  side 
from  the  wound  of  entry.  The  left  lower  limb  felt  "  dead,"  but  was 
capable  of  voluntary  movement.  The  sphincters  were  not  affected. 
When  he  was  admitted  to  hospital  a  week  later,  there  was  profuse 
haematuria,  apparently  of  renal  origin.  Three  weeks  after  the  injury, 
owing  to  the  presence  of  constant  pain  in  the  right  loin,  together  with 
fullness  in  the  region  of  the  right  kidney,  Mr.  Jocelyn  Swan  operated 
in  that  region  and  discovered  a  large  collection  of  clear  urine  around 
the  lower  pole  of  the  kidney,  which  had  been  lacerated.  A  bony 
spike  was  also  found  projecting  laterally  from  the  right  side  of  the 
body  of  the  3rd  lumbar  vertebra.  The  patient  made  an  uninterrupted 
recovery  from  this  operation,  and  no  further  renal  trouble  occurred. 

When  examined  eleven  days  after  the  original  wound,  there  was 
total  anaesthesia  and  analgesia  of  the  right  lower  limb  from  the  2nd 
lumbar  to  the  1st  sacral  root  areas  inclusive.     In  the  left  lower  limb 


ORGANIC    WAR-LESIONS 


553 


there  was  moderate  diminution  to  all  forms  of  sensation  in  the  dis- 
tribution of  the  5th  lumbar  and  1st  sacral  root  areas  (see  Fig.  282a). 
Joint-sense  was  lost  at  all  joints  of  the  right  lower  limb  from' the  hip 
downwards  ;  in  the  left  limb  it  was  lost  in  the  toes  only. 

There  was  total  flaccid  paralysis  of  the  right  lower  limb  at  all 
jomts.  The  left  lower  limb  was  feeble  at  all  joints,  but  no  individual 
movement  was  impossible.  Both  ankle-jerks  and  the  right  knee-jerk 
were  absent ;  the  left  knee-jerk  was  present.  The  plantar  reflexes 
were  absent.     The  sphincters  were  normal. 

To  faradism  the  right  calf  muscles  reacted  normally.  Theie  was 
no  reaction  in  any  other  muscles  of  the  limb,  from  the  glutei  down- 
wards.    All  the  muscles  of  the  left  lower  limb  reacted  briskly. 

About  a  month  after  the  original  wound,  the  patient  developed 


Fig.  282a. — Lesion  of  upper  cauda 
equina.  Anaesthesia  eleven) days 
after  the  injury. 


Fig.  282b. — The  same  case  as  Fig. 
282a.  Anaesthesia  eight  months 
after  the  injury. 


inveterate  pain  in  the  right  thigh,  chiefly  towards  the  inner  side  of 
the  knee  and  in  the  right  ankle.     This  persisted  for  many  months.     1 

Gradual  improvement  set  in,  both  as  regards  sensory  and  motor 
functions.  Eight  months  after  the  injury  the  ansesthesia  of  the  left 
limb  had  largely  cleared  up,  although  there  was  still  an  area  of  com- 
parative blunting  on  the  outer  side  of  the  leg  and  foot,  corresponding 
to  the  5th  lumbar  root.  In  the  right  lower  limb  the  ansesthesia  of  the 
2nd  sacral  area  had  receded  from' the  back  of  the  thigh  and  was  no 
longer  absolute  in  the  1st  sacral  area  (see  Fig.  282b).  An  area  of  intense 
cutaneous  hypersesthesia  persisted  at  the'  inner  side  of  the  thigh, 
corresponding  to  part  of  the  3rd  lumbar  area. 

Motor  power  also  returned,  completely  in  the  left  lower  limb  and 
partially  in  the  right.  The  glutei  and  adductor  muscles  were  the 
earliest  to  recover.  The  muscle  which  still  remained  severely  para- 
lysed was  the  quadriceps  extensor.     All  the  other  muscles  of  the  right 


554  NERVOUS   DISEASES 

lower  limb  had  recovered  voluntary  movement,  although  the  peronei 
and  dorsiflexors  of  the  ankle  were  relatively  weaker  than  the  rest. 
The  right  knee-jerk  and  both  ankle-jerks  were  still  absent,  also  the 
plantar  reflexes. 

Lesions  of  the  Lumbo-sacral  Plexus  and  of  its  Branches. — 

Compared  with  the  brachial  plexus,  the  lumbo-sacral  plexus  is  a 
comparatively  simple  affair.  Its  constitution  is  indicated  diagram- 
matically  in  Fig.  22  (p.  38).  Of  the  nerve-trunks  derived  from  the 
plexus,  the  largest  and  most  important  are  the  sciatic  and  the 
anterior  crural  nerve,  either  or  both  of  which,  especially  the  former, 
may  be  injured  from  plexus  lesions,  though  less  frequently  than 
from  direct  wounds  of  the  nerve  tininks  themselves. 

The  lumbar  portion  of  the  lumbo-sacral  plexus,  coursing  through 
the  substance  of  the  psoas  muscle,  is  more  often  affected  than  the 
sacral  part.  The  s}'mptoms  of  plexus  lesions  are  grouped  somewhat 
differently  from  those  which  result  from  peripheral  lesions. 

The  following  is  an  illustrative  example  of  a  lesion  of  the  3rd 
lumbar  root : — 

A  soldier  was  wounded  by  a  rifle  bullet  which  entered  half  an  inch 
below  the  upper  edge  of  the  right  iliac  crest,  five  inches  from  the  middle 
line.  There  was  no  exit  wound.  A  radiogram  showed  the  bullet  to 
be  lodged  in  the  right  side  of  the  body  of  the  4th  lumbar  vertebra.  The 
patient  immediately  lost  power  in  the  right  lower  limb,  and  for  three 
days  was  unable  to  make  any  movement  in  it.  Improvement  then 
set  in  rapidly,  beginning  at  the  foot  and  ankle.  "Within  three  weeks 
he  became  able  to  walk  with  a  stick.  He  complained  of  occasional 
pains  along  the  inner  side  of  the  right  thigh,  from  groin  to  knee,  also 
of  loss  of  feeling  in  the  region  of  the  knee. 

When  examined  a  month  after  the  injury,  there  was  an  area  of 
complete  anaesthesia  to  all  forms  of  stimuli  on  the  front  and  outer 
side  of  the  right  thigh  and  along  a  narrow  strip  at  the  inner  side  of 
the  knee  (see  Fig.  283). 

There  was  complete  paralysis  of  the  right  quadriceps  extensor, 
and  some  weakness  of  the  flexors  and  adductors  of  the  hip.  All  the 
other  muscles  of  the  lower  limb  were  powerful.  To  faradism  there  was 
loss  of  reaction  in  the  quadriceps,  with  diminution  in  the  adductor 
muscles. 

The  right  knee-jerk  was  absent  ;  the  left  was  brisk.  Both  ankle- 
jerks  were  normal. 

The  next  case  is  one  in  which  the  5th  lumbar  root  was  damaged, 
its  motor  fibres  being  exclusively  affected  : — 

A  soldier,  aged  twenty-one,  was  wounded  by  a  shrapnel  bullet 
which  entered  half  an  inch  to  the  left  of  the  £th  lumbar  spine.     There 


ORGANIC   WAR-LESIONS 


555 


was  no  wound  of  exit,  but  the  bullet  lodged  (as  shown  by  a  radiogram) 
in  the  lower  part  of  the  body  of  the  2nd  lumbar  vertebra,  in  the  middle 
line.  The  patient  was  standing  at  the  moment  of  being  hit,  and  im- 
mediately dropped  backwards,  his  legs  giving  way.  The  left  lower 
limb  was  immediately  paralysed,  whilst  the  right  limb  felt  slightly 
weak  for  a  few  hours. 

Within  two  days  he  began  to  recover  power  in  the  left  hip  and 
knee,  but  had  not  regained  power  of  dorsiflexion  of  the  left  ankle. 
He  had  a  subjective  sensation  of  numbness  along  the  back  of  the  left 
thigh  and  at  the  back  and  outer  side  of  the  left  leg.  There  was  never 
any  affection  of  sphincters. 

On  examination  two  and  a  half  weeks  after  the  injury,  there  was 


Fig.  283. — Anaesthesia  in  a  case  of  lesion  of  the  3rd  lumbar  root. 


no  loss  of  sensation  to  any  form  of  cutaneous  or  deep  stimulation  ; 
joint  sense  was  everywhere  normal. 

The  right  lower  limb  was  normal.  In  the  left  lower  limb  the 
movements  of  the  hip  and  knee  were  powerful.  Flexion  of  the  toes 
was  also  normal.  There  was  paralysis  of  the  anterior  tibial  and 
peroneal  groups  of  muscles,  so  that  dorsiflexion  and  eversion  of  the 
ankle  were  impossible,  and  he  had  drop-foot.  The  knee-jerks  and 
ankle-jerks  were  brisk  and  equal.  To  faradism  there  was  diminution 
of  reaction  in  the  peronei  and  anterior  tibial  groups. 

In  a  work  like  this,  space  does  not  permit  the  full  discussion 
of  the  syniptomatology  of  paralysis  of  the  individual  nerves  of 
the  limbs.  The  diagnosis  of  such  lesions  is  dependent  mainly  on 
an  accurate  knowledge  of  anatomy.  A  few  main  facts,  however, 
may  here  be  mentioned,  applicable  to  peripheral  nerve  lesions  in 
general. 


556  NERVOUS   DISEASES 

Within  the  peripheral  nerves  the  fibres,  whether  sensory  or 
motor,  are  arranged  just  as  definitely  with  relation  to"  each  other 
as  are  the  fibres  in  the  cervico-brachial  or  lumbo-sacral  plexuses. 
The  fasciculi  within  the  peripheral  nerves  do  not  run  haphazard, 
but  occupy  certain  definite  relative  positions  within  each  nerve- 
trunk.  Thus,  for  example,  in  the  ulnar  nerve  at  the  bend  of  the 
elbow,  the  fibres  destined  for  the  interosseal  muscles  of  the  hand 
he  superficially,  whilst  those  destined  for  the  ulnar  half  of  the  flexor 
profundus  and  for  the  adductor  polhcis  lie  deeply,  close  to  the 
humerus.  Again,  in  the  sciatic  nerve,  in  the  gluteal  region,  not 
only  can  we  distinguish  the  internal  popliteal  fibres,  lying  inter- 
nally, from  the  external  popliteal  fibres  externally  (indeed  they 
sometimes  constitute  two  parallel  but  separate  nerves),  but  the 
cutaneous  fibres  of  the  external  saphenous  and  internal  plantar 
branches,  together  with  the  muscular  branches  for  the  cah  muscles, 
are  situated  internally,  whilst  the  fibres  of  the  external  plantar 
nerve,  together  with  the  muscular  branches  for  the  tibialis 
posticus  and  the  long  flexors  of  the  toes,  lie  externally.  Thus 
a  lesion  of  the  outer  part  of  the  sciatic  trunk,  high  up,  often 
produces  paralysis  limited  to  the  external  popliteal,  whilst  a 
partial  lesion,  lower  down,  may  produce  a  paralysis  limited  to  the 
long  flexors  of  the  toes  and  of  the  tibiahs  posticus,  accompanied 
by  an£esthesia  of  the  outer  border  of  the  foot. 

Ischaemic  Myositis.— We  have  already  referred  to  the  ordinary 
variety  of  ischsemic  myositis  due  to  the  pressure  of  tight  splints 
or  bandages  (see  p.  247).  In  the  present  war,  however,  another 
type  of  ischsemic  myositis  has  been  occasionally  met  with,  result- 
ing from  direct  injury  of  the  artery  supplying  the  muscle  group 
and  without  the  occurrence  of  any  pressure  on  the  muscles  them- 
selves.    The  following  is  an  illustrative  example  : — 

A  soldier,  aged  twenty-two,  was  wounded  in  the  left  upper  arm. 
The  entry  wound  was  through  the  middle  of  the  biceps  ;  the  exit  was 
at  the  same  level,  an  inch  behind  the  brachial  vessels  and  nerves. 

When  admitted  to  hospital  ten  days  later,  there  was  a  considerable 
swelling  in  the  upper  arm,  and  no  pulse  could  be  felt  at  the  wrist. 
There  was  weakness  of  the  wrist  and  fingers.  No  splint  or  bandage 
was  applied  to  the  forearm  at  any  period  of  the  treatment. 

On  the  thirteenth  day  after  the  injury,  secondary  heemorrhage 
occurred  from  the  wound  of  exit.  The  false  aneurism  was  accordingly 
laid  open,  the  blood  clot  was  turned  out,  and  the  vessels,  above  and 


ORGANIC    WAR-LESIONS  557 

below  the  aneurism,  were  ligatured.  Uninterrupted  recovery  took 
place  from  this  operation. 

On  the  day  after  the  operation,  some  return  of  power  was  observed 
in  the  extensors  of  the  wrist  and  fingers.  Improvement  steadily 
continued,  but  the  flexors  of  the  wrist,  fingers,  and  thumb  remained 
permanently  paralysed,  and  gradually  the  paralysed  muscles  developed 
a  curious  hard,  doughy  consistence.  All  the  other  muscles  of  the  upper 
arm,  forearm,  and  hand  were  normal. 

Two  months  after  the  original  injury,  the  motor  disability  remained 
unchanged.  To  pin-pricks  there  was  analgesia  of  the  hand  from  the 
wrist  downwards.  To  cotton-wool  touches,  anteriorly  there  was  an- 
aesthesia below  a  level  two  inches  above  the  wrist,  whilst  posteriorly 
sensation  was  lost  only  from  the  knuckles  downwards.  Small  blisters 
formed  occasionally  on  the  dorsal  aspect  of  the  terminal  phalanges. 

No  reaction  to  faradism  or  galvanism  could  be  obtained  in  the 
paralysed  long  flexors  of  the  wrist,  fingers,  or  thumb,  even  under  a 
general  anaesthetic,  whereas  all  the  other  muscles  of  the  limb  reacted 
in  normal  fashion. 

Similar  ischseniic  palsy  is  sometimes  observed  in  the  lower 
limb.  Thus,  after  ligature  of  the  femoral  artery,  paralysis,  with 
doughy  hardness  and  loss  of  electrical  reactions,  has  occasionally 
been  observed  in  the  anterior  tibial  and  peroneal  groups  of  muscles. 
We  note  in  such  cases  that  no  injury  has  been  inflicted  on  the  nerve- 
trunks  ;  the  condition  is  therefore  circulatory  in  origin. 


INDEX 


Abadie's  sign  of  tahes,  203,  213 
Abdomen — 

motor   points   of    wall    (Eib's   dia- 
gram), 417 
Abdominal    reflex — significance    of    ab- 
sence, 332 
Abdominal  sympathetic,  diseases  of — 

pigmentary      changes,      cutaneous, 
369 

visceral  disorders,  368,  369 
Abductor  palsy  of  larynx,  175,  176 
Abscesses  of  brain,  484,  496 

aphasia  from,  109 

cerebro-spinal  fluid  in,  440 

fits  due  to  cortical,  81 

headache  due  to,  183 
Absinthe-poisoning,    coma   and  convul- 
sions from,  79 
"  Acetone  "  breath,  71 
Achilles-jerk,  339 
Achromatopsia,  132 
Acromegaly,  132,  306,  476 

transient,  in  pregnancy,  32 
Acro-parfflsthesia,  371 
Active  muscle-sensation,  198 
Addison's  disease,  369 
Adductor  paralysis  of  larynx,  176 
Adiposis   dolorosa    (Dercum's    disease), 

305 
Adipose-genital  dystrophy,  476 
Aerophagy,  411 
Afferent   impulses,     2,    13,    14   et  seq.  ; 

path  of,  14,  16;  diagrams,  15,  18 
Ageusia,  153 
Agnosia,  116 
Agoraphobia,  383 
Agraphia,  108,  113,  115 
Aichmophobia,  383 


Air-swallowing,  411 
Akinesia  algera,  197 
Albinism,  nystagmus  in,  144 
Albumin,  excess  in  cerebro-spinal  fluid, 

435 
Albuminuria,  orthostatic,  369 
Alljuminuric  retinitis,  diagnostic  signifi- 
cance, 79 
Alcoholism — 

amblyopia  of,  132 

articulation  in,  122 

ataxia,  278 

coma  and  convulsions,  70,  79 

facial  pai^alysis  in,  163 

factor  in  nervous  disease.  58 

gait  in,  299 

insomnia  in,  460 

men  and  women,  effects  in,  58 

neuritis  from,  58  ;  multiple  neuritis 
from,  214,  243 

paralysis.     See  Xeuritis 

Quinquaud's  sign,  93 

toxic  vertigo,  169 

tremor,  92 
Alexia,  112 

Allocheiria,  201,  204,  400 
"  AUongement  croise,    phenomene   d'," 

230 
Alopecia,  319 

Alternate  paralysis,  218,  225,  482 
Amaurosis,  397-399 .     See  also  Blindness, 

hysterical 
Amaurotic  family  idiocy,  135 
Amblyopia,  crossed,  45 

in    hysteria,    132,     397,    398  ;     in 
tumours,  472 

after  shell  explosions,  399 
Amblyopia,  tobacco,  130,  131 
Ambulatory  automatism,  78,  402 


559 


560 


NERVOUS  DISEASES 


Ammonium  sulphate  test  for  globulin, 

435 
Amnesia  retrogade,  62 
Amyotonia  congenita,  291-292 
Amyotrophic  lateral  sclerosis,  89,  121, 

231,  235,  341 
Ansemia — 

cerebral,  causing  vertigo,  168  ;  and 
sleep,  451,  453 

headache  of,  183,  185 

mydriasis  in,  137 

optic  neuritis  in,  135 

primary  thrombosis  of  sinuses  in, 
68 

tinnitus  in,  167 
Anaesthesia — 

auto-exploration  of  sensibility,  201 

cortical,  208 

crossed,  17 

cutaneous,  41,  199-202 

dissociated,  204,  211 

hemi-ansesthesia.     See  that  title 

hysterical,  206,  391-397  ;  mode  of 
disappearance,  396  ;  diagrams, 
393,  397 

leprous,  214 

mapping  of  areas,  199,  202 

para-ansestliesia,  209 

in  peripheral  neuritis,  196 

in  peripheral  palsies,  213 

spinal,  after-effects,  450 ;  contra- 
indicated,  450  ;  mode  of  induc- 
ing, 447-450 

of  spinal  lesions,  209 
incomplete,  210 

tabetic,  212 

tactile,  204 

thermo  ,  204,  210 

in  tubercula  dolorosa,  197 

universal,  of  hysteria,  206 
Anesthetics,  delayed  poisoning  by,  72 

spinal,  examples   of  solutions,  447 
note 
Anal  reflex — 

internal,  346,  349 

superficial,  331,  335 
Analgesia,  204,  212 

in  tabes,  204,  212 
Anarthria,  articulative,  108,  115 
Aneurisms,  intra-cranial,  166,  484 

pulsating  sounds  with,  167,  453 


Angina  pectoris,  190,  368 
Angio-neuroses,  58,  369-377 
Angio-spastic  hemiplegia,  265 
Anidrosis,  localised,  364,  375 
Anisocoria,  136 
Ankle-clonus,  221,  296,  342  ;    inhibition 

of,  229  ;  spurious,  221,  343,  409 
Ankle-jerk,  336,  339 
Ankylostomiasis,  457 
Anorexia  nervosa,  304,  411 
Anosmia,  57,  84,  128,  155  ;  with  brain 

tumours,  469 
Anterior  cornua,  cells  of,  2,  3,  34,  89 

deep  reflexes,  loss  of,  341 

lesions,  89,  232,  233-236 

motor  palsy  in,  232,  234 

motor  tract  through,  2,  34 

posture  in  muscular  paralysis  from, 
280 
Anterior  crural  paralysis,  240-242 
Anterior  nerve  roots.     See  Spinal  Nerves 

— Roots 
Anterior       polio  -  myelitis        (infantile 
paralysis) — 

acute,  233 

chronic,  234 

loss  of  deep  reflexes  in,  341 
Anterior  transverse  gyrus  of  Heschl,  47, 

48,  107,  471 
Anthropophobia,  383 
Antrum    of    Highmore,     empyema    of, 

129 
Anuria,  hysterical,  412 
Aphasia,  106  et  seq. 

auditory,  107,  111,  471 

cortical   centres   involved   in    (dia- 
grams), 107,  109,  113 

dysarthria  distinct  from,  119 

functional,  or  temporary,  109 

hysterical,  114 

lachrymosity  in,  58 

Marie's  views,  115 

motor,  108,  114,  469 

scheme  for  investigation  of,  110 

sensory,  107,  108,  111-114,  115 

total,  115 

visual.     Sec  that  title 
Aphemia,  108 

Aphonia,  hysterical,  125,  176,  388,  413 
Apoplexy,  diagnosis  of,  63,  434 
Appendicitis,  pseudo-,  412 


INDEX 


561 


Apraxia,  116 

in  callosal  tumour,  474 

in     relation     to     corpus     callosuni 
(diagram),  117 

mode  of  testing  for,  116 
Arachnoidal  sac,  430 
Argyll-Robertson  pupil,  136,  139 
Arm,  cerebral  paralysis  of,  7 

sensory  fibres  from,  20 
Arsenical  poisoning — 

cutaneous  affections,  317 

multiple  neuritis  due  to,  243 
Arteries — 

cerebellar,  51 

cerebral,  48,  51 

diseases  of,  64 

of  spinal  cord,  52 
Arthropathies,  323-329 
Articulation,  disorders  of,  119- 127 

alcoholic,  122 

ataxic,  122 

in  bulbar  palsy,  121 

deaf-mutes,  126 

in  disseminated  scleroeis,  124 

functional  cortical  disturbance,  124 

in  general  paralysis  of  insane,  122 

hysterical,  125,  389 

idioglossia,  127 

infra-nuclear  and  nuclear  affections 
of,  120 

lalling  and  lisping,  126 

stammering,  124,  389 

supra-nuclear  affections  of,  122 

tests  of,  119 

tics  of,  125 
Articulation  distinguished  from  speech, 

119 
Asphyxial  convulsions,  79,  82 
Associated  movements,  97,  223 
Astasia-abasia,  297,  408,  413 
Astereognosis,  203  ;  with  brain  tumour, 

472 
Asthenic  bulbar  paralysis   (myasthenia 

gravis),  260 
Asthma,  dyspncea  of,  370 
Astigmatism,  headache  of,  184 
Asynergia,  276,  277,  478,  479 
Ataxia,  269 

alcoholic,  278 

cerebellar,  276 

in  disseminated  sclerosis,  272,  278 


Ataxia  (cwitinual) — 

Friedreicli's,  273 

hereditary  cereliellar,  276 

olivo-ponto  cerebellar,  27G 

tabetic,  271 

vestibular,  272 
Ateleiosis,  476 
Athetosis,  57,   96,  278  ;  bilateral,  123  ; 

figures  of  case,  97 
Atopognosis,  201 

Atrophy,  acute  yellow,  ooma  of,  72 
Atrophy,  muscular,  217,   248  ;   in  hys- 
teria,   259,  409  ;     Werduig-Holf- 
mann  type,  236 

progressive,  234 
Auditives  and  visuals,  108 
Auditory  aphasia,  107,  111,  115 

of  brain  tumour,  471 

cortical  and  sub-cortical.  111 
Auditory  centre,  47,  107-109 
Auditory  gyrus  (Fleclisig),  47,  109 
Auditory  nerve,  affections  of,  and  tests, 

165 
Auditory  path,  47 
Auditory  word  centre,  107 
Aura  preceding  epilepsy,  75 
Auriculo-ventricular    muscle-bundle    of 

Kent  and  His,  83 
Auto-exploration  .of  cutaneous  sensation, 

201 
Automatic   movements,   conjugate,    98, 

295 
Automatism,  4 

ambulatory,  78 

hysterical,  402 

post-epileptic,  78 
Autonomic  nervous  system,  352,  353 

lesions  of,  369,  370 

relation  to  drugs  and  glands,  356 

vagal    fibres    of,     172,     173,     353, 
355 
Avellis's  syndrome,  173 


B. 

Babinski's  combined  flexion  of  hip  and 
trunk,  220 ;  extensor  plantar  reflex, 
332-334 

Barany's  pointing  tests,  24,  272 

Barany's  thermic  nystagmus,  142 

Basilar  artery,  48 


662 


NEKVOUS  DISEASES 


Bastian's  law,  345 
Becliterew-Mendel  reflex,  344 
Bed-sores,  58,  247,  311-313;  absence  of 

in  hysteria,  413 
Bell,  nerve  of,  242 
Bell's  paralysis,  158-160 
Benedikt's  syndrome,  95,  225,  476 
Beri-beri,  243 
Biceps  muscle — 

atrophy     from     anterior     cornnal 
lesion,  282 

innervation  of,  41 

reflex,  336 
Biernacki's  sign  in  tabes,  212 
Birth  convulsions,  83 
Bi-temporal  hemianopia,  132 
Bladder — 

disorders  due  to  lesions  of  cord  or 
Cauda  equina,  347-348 

dribbling  from,  348 

in  hysteria,  410 

innervation,  347-348 

reflex  centres  for  contraction,   347- 
348 
"  Bleeding  diseases,"   cerebral   hsemor- 

rhage  in,  65 
Blepharospasm,  102,  403 
Blindness,  in  amaurotic  family  idiocy, 
135 

hysterical,  397-399 

lesions  causing,  45 
Blood-pressure  in  coma,  64 

effect  of  pituitary  secretion  on,  32 
Blood-vessels — 

angio-neuroses  affecting,  369-377 
Blue-blindness,  132,  463 
Blue  oedema,  hysterical,  413 
Bones — 

brittleness  in  disease,  322 

convulsions     following      injury    of 
cranial,  81 

sensory  fibres  from,  19 

trophic  changes  in,  321-323 
Borborygmi,  411 
Brachial  neuralgia,  192 
Brachial  paraplegia,  218 
Brachial  plexus,  lesions  of,  362  ;  wounds 
of,  544-551 

axillary,  544,  548,  549 

peripheral,  544 

supraclavicular,  544,  546,  547 


Brain — 

abscess  of,  81,   109,   183,  440,  484, 

496 
aiifemia  of,  168,  451 
anatomy  and  physiology  of,  1-54 
arterial  supply,  48-52 
circulation  in,  arterial,  48  ;   venous, 

52 
concussion  of,   62  ;    headache  after, 

185 
cortex,  histology  of,  6 
hasmorrhage.       See   under   Htemor- 

rhage,  cerebral 
hypertemia  of,  168 
injuries,  focal  signs  of,  498-512 
cerebellar,  511,  512 
frontal,  508,  509 
occipital,  506-508 
parietal,  510,  511 
post-central,  502-503 
precentral,  498-502 
pre-  and  post-central,  503-506 
temporal,  509,  510 
lesions,  palsies  due  to,  7-10 
localisation  of  function,  6-11 
membranes,  innervation,  181 
motor  areas,  localisation  of,  6 
sensory  tracts  in,  18 
traumatic  hemorrhage  with  "com- 
pression," 65 
tumours.        See    under     Tumours, 

intra-cranial 
wounds  of,  487-512 

pathological  results — 
abscess,  496 
hsemorrhage,  493 
hernia  cerebri,  497-498 
meningitis,  497 
cedema,  496 
optic  neuritis,  498 
protective     coverings     of. 

487,  488 
softening,  495 
Breathing — 

in  cerebral  concussion,  62 
in  cerebral  hfemorrhage,  64 
in  diabetic  coma, 72 
in  hysterical  trance,  72 
"  Breites  Bein,"  Heilbronner's,  287 
Brissaud's  reflex,  333 
Broca,  cortical  centre  of,  51, 107, 108,  115 


INDEX 


563 


Brown-Sequaid    paralysis,  11,    21,   'AO'i, 
204,  210,  228,  523-524 
diagram  of  symptoms,  21 
lirudziuski's  signs  of  meningitis.  68 
Bulbar     palsy     (glosso-labial-laryngeal 
paralysis),    121  ;    unilateral   syn- 
drf)me,  275 
articulation  in,  121 
lachrymosity  in,  58 
mixed  electrical  reactions  in,  427 
pseudo-,  123,  226 
tongue  tremors  of,  89 
Bulbar  phenomena  in  Meniere's  disease, 

170 
Bulbo-cavernosus  retiex,  331,  335 

C. 

Cadaveric  reaction,  266,  424 
Caisson  disease,  195 

Calcarine  fissure,  45  ;  lesions  of,  134,  473 
Calmette's  ophthalmo-reaction,  485 
Capsule,  internal,  anatomy  of,  7 

motor  fibres  of,  7 
Carcinoma  of  brain,  463  ;  coma  of,  72 
Caries  (dental) — 

headache  due  to,  183 
neuralgia  due  to,  188 
Caries,  spinal,  root  pains  with,  196 
Carotid    artery,    hemiplegia   following 

ligature  of,  512-514 
Carpo-metacarpal  reflex,  336 
Case-taking,  method  of,  56-60 
Catalepsy,  77,  401 

cerebellar,  31,  480 
Cataract  as  cause  of  nyctalopia,  130 
and  tetany  of  gastric  origin,  86 
Catheterisation,  rigor  following,  88 
Cauda  equina^ 

lesions  of,  244-247,  528-529,  551-553 
anal  anaesthesia  from,  349 
bladder  trouble  in,  348 
bulbo-cavernosus  reflex,   loss  of, 

335 
bullet  wounds  of,  246,  528,  551 
gait  in,  300 

motor  paralysis  due  to,  245 
recto-perineal  pain  in,  196,  247 
relations    with     vorteljral     column 
(diagram),  430 
Caudate  nucleus  (diagrams),  8,  9 


Cavernous  sinus,  thrombosis  of,  54 
Cells,  nerve,  physiology  of,  1 
Central  scotomata,  131 

for  colours   in  tobacco  amblyopia, 

130,  131 
in  migraine  (transient),  131 
in  retrobulbar  neuritis,  135 
•  Cerebellar  catalepsy,  31,  480 
Cerebellum — 

anatomy  and  physiology  of,  20-28 

arterial  supply,  52 

ascending  tracts  in  connection  with, 

36 
ataxia,  or  asynergia,  30,   276,  277, 

478,  479 
cerebello-fugal  fibres  of,  26,  28 
cerebello-petal  fibres  of,  25 
connections  of  (diagram),  23 
cortex,    low    excitability    of,     28  ; 

motor  centres  in,  29 
destruction,  results  of,  30 
equilibration,    co-ordinating  centre 

for,  28,  167 
indirect  action  on  spinal  cord,  28 
intoxication  of,  122,  278 
lesions  of — 

ataxia  due  to,  270,  276-277 
attitude  in  (fig.).  299,480 
dysdiadocho-kinesia  with,  277, 

479 
fits  due  to,  86,  480 
forced  rotatory  movements,  479 
gait  in,  299 
motor  effects,  28,  29 
nystagmus  in,  144 
skew  deviation  of  eyes   from, 

148,  480 
vertigo  in,  167,  169 
wounds  of,  511-512 
lobes  of,  23-25 
nuclei  within,  25 
pedimcles  of,  25,  167 
pointing  tests  in  lesions  of,  29,  272, 

273 
section  through  (diagram),  26 
stimulation,  results  of,  30 
tracts  leading  to  and  from,  25-28 
tumours  of,  169,  186,  299,  478-480 
Cerebral  ataxia,  278 

Cerebral  sinuses,  thrombosis  of,  46,  54, 
68 


564 


NEKVOUS  DISEASES 


Cerebral.      See    also    under    Abscesses, 

Brain,  Hfemorrhage,  and  Tumours 
Cerebro-spinal  fluid,  57,  429-450 
bacteria  in,  438 
cells  of,  434,  440 

in  cerebro-spinal  syphilis,  442-444 
chemical  characters,  435 
coagulation,  massive,  in,  435 
colloidal  gold  reaction  of,  436-438 
cytology  of,  440 
lymphocytosis  in,  79,  189,  267,  311 

note,  440 
microscopic  examination  of,  439 
parasites  in,  439 
permanganate  reaction  of,  436 
physical  characters  of,  434 
pleocytosis  in,  440 
in  polio-encephalitis,  83 
in  polio-myelitis,  441 
pressure  of,  432 

puncturing  for.     See  Thecal  punc- 
ture 
source  of,  429 
tumour  cells  in,  440 
Wassermann  reaction  in,  436 
xanthochromia  of,  435 
Cervical  plexus,  36,  37 
Cervical  region  of  cord  — 
lesions  in,  137,  218,  226 
muscular  localisation  in,  41 
Cervical  sympathetic — 

course  and  distribution,   135,    151, 

178,  357 
in  diagnosis,  58 
excision  of,  365 
lesions,  358,  543 
oculo-pupillary    fibres,     course     of 

(diagram),  358 
paralysis  of — 

from   brachial   plexus  rupture, 

362 
from  tumour,  361 
symptoms  of,  358-360 
stimulation,  clinical,  360,  366 
sweat-fibres  supplied  by,  364 
Charcot's  "  grande  hysteric,"  401 

"  migraine  ophthalmoplegique,"  151 
tabetic  joints,  323 
Charcot  and  Marie's  progressive  neuritic 

amj'otrophy,  236 
Chemosis,  54 


Chloral  poisoning,  tremor  in,  92 
Chloroma,  cerebro-spinal  fluid  in,  441 
Chorda  tympani,  153,  157,  160,  164 
Chorea,  96 

articulative  defects  in,  124 

ataxia  in,  278 

bed-sores  in,  313 

gait  in,  302 

Huntington's,  96 

hyoscine,  96 

rheumatic,  96 

tic  distinct  from,  101 
Choroid  artery,  anterior,  49 
Chvostek's  sign  of  tetany,  85,  86 
Cigarette  smoking,  toxic  effects  of,  92 
Ciliary  ganglion,  136,  149 

degeneration,  149  ;  diagram,  138 
Ciliary  muscle,    innervation,  136  ;  dia- 
gram, 138 
Cilio-spinal  centre  (diagram),  358 

reflex,  58,  346,  360 
Circumflex  nerve,  36 
Circumvallate  papillae,  153 
"  Claudication  intermittente  "— 

arterial,  195,  197,  263,  374 

cerebral,  265 

spinal,  264 
Claustrophobia,  383 
Clavus  hystericus,  186,  389 
Claw  hand,  283 
Clonus,  342-344 

inhibition  of,  342 

pseudo-clonus,  343,  407 
Cocaine — 

injection  by  thecal  puncture,  447 

ocular  phenomena  produced  by,  137, 
366 

tremor  due  to,  92 
Coccygodynia,  192 
Cochlear     fibres,     auditory    nerve,    48, 

164 
Cochlear   and   vestibular  nerve  connec- 
tions (diagram),  48 
Coffee  and  tea  poisoning,  tremor  in,  92 
Colitis,  muco-membranous,  369 
Colour-blindness,  130 
Colour  vision,  tests  for,  130 
Coma,  62-73 

of  acute  yellow  atrophy,  72 

of  alcoholic  intoxication,  70 

bladder  trouble  in,  348 


INDEX 


565 


Conia  {contiuAccd) — 

carcinoniatosum,  72 

from  cerebral  concussion,  62 

from  cerebral  liK;morrliage,  63 

from  cerebral  meningitis,  08 

from  chronic  subdural  hiemorrliage, 
65 

diabetic,  71 

ocular  tension  in,  72 

diagnosis  and  causation,  62  ct  seq. 

hysterical  trance  and,  72 

malarial,  72 

of  opium  poisoning,  70 

of  pontine  haemorrhage,  67 

post-epileptic,  71 

and  sleep,  426 

in  Stokes-Adams'  syndrome,  71 

in  sunstroke,  72 

in  thrombosis  of  cerebral  sinuses,  68 

toxfemic,  69 

from  traumatic  cerebral  compression , 
65 

urseraio,  71 
Comminuted  cranial  wounds,  491 
Compression,  cerebral,  65,  493 

of  spinal  cord  in  Avounds,  516 
Concussion  of  brain,  62,  492 

headache  after,  185 
Condenser  discharges  in  electrical  reac- 
tions, 425 
Conditional  reflexes,  41,  349 
Congenital  ptosis,  150 
Conjugate  automatic  movements,  98,  295 

in  hemiplegia,  98 

in  diplegia,  98,  295 
Conjugate  deviation,  9,  148,  469 
Conjunctiva^ 

anfesthesia   in  fiftli  nerve  paralysis, 
153 

conjunctival   reflex.      See   Reflexes, 
corneal 

nerve-supply,  151,  152 
Consciousness,  double,  382,  401 
Consonants,  articulation  of,  122,  126 
Constipation — 

occipital  headache  of,  185 

spastic,  369 

toxic  vertigo  from,  170 
Contractures,  hysterical,  409 

organic,  222,  285-287,  345 
Cunus  meduUaris,  lesions  of,  246 


Convulsions,  74-87 

generalised  epileptiform,   with  cere- 
bral tumours,  464 
infantile,  82 
strychnine,  84 
See  also  Fits  and  Epilepsy 
Coprolalia,  101 
Copropliobia,  383 
Corneal  reflex.     See  Reflexes 
Corona  radiata,  7 
Corpora  dentata,  25 

Corporaquadrigemiua,  14, 45,  47, 136, 475 
Corpus  callosum — 

relation  to  apraxia  (diagram),  117 
tumours  of,  474 
Cortex  cerebri — 

arterial  supply  of,  50,  51 
diagrams  of,  5 
lesions— 

anaesthesia  due  to,  208 
fits  in,  80-82 

motor,  inco-ordination  in,  278 
motor  palsy  from,  7,  224 
venous  supply,  52 
Cortical  auccsthesia.    See  Anaesthesia 
Cortical  cells  in  sleep,  452 
Cortical  centres — 
auditory,  47,  107 
half-vision,  45,  46,  ^12-ilZ 
of  hunger  and  thirst,  48 
motor,  4-8 
olfactory,  44 
sensory,  5,  208 
of  speech,  107-109  ;  diagrams,  107, 

109  ;  mal-development,  126 
of  taste,  47 
of  vision,  45 
of  writing,  108 
word -blindness,  103 
Cortical  localisation  (diagrams),  5 
Cortico-spinal   motor    neurone     lesions. 

See  Motor  paralyses 
Cough,  hysterical,  413 
Craft  palsies  and  cramps,  265 
Cramp,  267 
Cranial  bones,  headache  from  aff'ections 

of,  183 
Cranial  nerves — 

Abducens  (Sixth),  135  ;  lesions  of, 
1],  135  ;  paralysis  of,  11,  55,  147, 
466,  482 


566 


NERVOUS  DISEASES 


Cranial  nerves  (continued) — 

Auditory  (Eighth),  164-172  ;  coch- 
lear division,  47,  164  ;  diagrams 
of,    129,    130  ;    vestibular   fibres, 
164 
Facial  (Seventh),  157-164 

lesions  at  different  levels,  157- 

164 
motor  root,  158  164 
secretory     and     taste     fibres, 
course  of,  47,  152,  158,   161, 
164 
sensory  root,  47,  164 
wounds  of,  542,  543 
Glosso-pharyngeal  (Ninth),  47,  153, 
172 
course  of  taste-fibres  (diagram), 
152 
Hypoglossal  (Twelfth) ,  178,  180 
paralysis,   178  ;  unilateral,  120, 
543 
Nervus  intermedins    of    Wrisberg, 

47,  164 
Oculu-matorius  (Third),  135 

paralysis  of,    95,   144-146,    225, 
476,  541 
Olfactory  (First),  44,  128-129 
Optic  (Second),  45,  129 
Patheticus   (Fourth),  135  ;   paraly- 
sis of,  54,  146 
Recurrent   laryngeal,    paralysis   of, 

120,  173,  174,  175 
Short  ciliary  nerves,  138 
Spinal  accessory   (Eleventh),    177  ; 

paralysis,  177,  178 
Trigeminal  (Fifth),   151-156 

cutaneous    supply,  to   head  (dia- 
gram), 151 
distribution,  151,  153 
incidence  of  rodent   ulcers  over, 

314 
lingual  branch  of,  152,  153 
ophthalmic    division,    lesion    of, 

358 
pains  in  region  of,  187 
paralysis  of,  153-156,  542 
sensory  root  of,  17,  47 
sweat   areas    corresponding  with 

distribution  of,  376 
taste  fibres,  course  of  (diagram), 
152 


Cranial  nerves  (continued)  — 

Vagus   or    Pneumogastric    (Tenth), 
172 
autonomic  fibres  of,  172,  353 
paralysis,  173-177,  542 
Vidian  nerve,  151 
wounds  of,  540-543 
Cranio-cerebral  topography,  4 
Cranium,  fractures  of — 
comminuted,  491 
compound,  490 
depressed,  489 
fissured,  489,  490 
gutter,  489 
punctured,  489 
Cremasteric  reflex,  331,  335 
Crimes,    in    post-epileptic    automatism, 

78 
Crossed  amblyopia,  45,  132 
in  hysteria,  132,  397 
in  tumours,  472 
Crossed  anaesthesia,  17 
Crossed  hemi-ansesthesia,  19,  209 
Crossed  paralysis,  11,  57,  218,  482 
Cms  cerebri^ 

lesions  of,  10,  95,  225,  476 
motor  palsy  due  to,  225 
tegmental  region,  95 
Cuneate   lobule,    visual  half-centres   in, 

lesions,  134 
Cutaneo-gastric  reflex,  346 
Cutaneous  sensibility,  15,  199-202 
loss  of.    See  Aufesthesia 
recovery  of,  242 
Cyanosis,  local,  in  anterior  poliomyeliiis, 
375 
in  erythromelalgia,  372 
in  Raynaud's  disease,  371 
Cysticercus    in   fourth   ventricle,    diag- 
nosis, 169 
cerebrospinal  fluid  with,  169 
Cyto-diagnosis   of  cerebro-spinal    fluid, 
440-444 

D. 

Dartos  reflex,  349,  446 
Deaf-mutism — 

in  children,  126 

as  war  neurosis,  126 
Deafness,  161,  164-166,  170-171,  475 

due  to  drugs,  167 


INDEX 


567 


Decerebrate  rigidity,  98 

posture  in,  93 
Deconipicssion  paraplegia,  195 
Decubitus,  acute,  312 
Det'iccation,  'Aid,  330,  349 
"  Defensive"  reflexes,  229 
Degeneration,  ascending,  36 

descending,  34,  35 

progressive  lenticular,  95 

of  spinal  cord,  combined,  272,  345 
,  AVallcrian,  36 
Deiters'  nucleus,  25,  28 

focal  lesion  of,  171 
Delirium,  58 
Delirium  tremens,  58,  92 
Deltoid,  atrophy  of,  233,  238 

paralysis     from     anterior     cornual 
lesion,  281 

])aralysis  of,  from  lesion  of  circum- 
flex, 36 
Dementia,  bedsores  in,  312 
Dementia  paralytica.     Sec  General  para- 
lysis 
Depressed  fractures  of  cranium,  489 
Dercirm's    disease    (Adiposis    dolorosa), 

305 
Dermatomes,  38 
Dermographism,   146,  373  ;  in  liysteria, 

413,  414 
Diabetes — 

bilateral,  tic  douloureux  in,  187 

breath  in,  71 

coma  of,  71 

insipidus,  369 

multiple  neuritis  due  to,  243,  310 

optic  neuritis  in,  135 

perforating  ulcers  in,  310 
Diadochokinesia,  277,479 
Diaphragm,  myoclonus  of,  89 
Diarrhcea,  hysterical,  412 

paroxysmal,    of    Addison's  disease, 
369 
Dilator  pupillse,  137,  151,  359 
Diphtheria,  neuritis  after,  140,  243 
Diplegia,  96,  218,  226,  295 

causes  of,  7 

conjugate  automatic  movements  in, 
98 

definition  of,  218 

silastic,  295 
Diplococcus  intra-cellularis,  438 


Diplopia,  141,  147 

false  image,  position  of,  141,  147 

gait  with,  299 

monocular  (hysterical),  400 

ocular  vertigo  with,  170 

tests  for,  141-142 
Di[)8omania,  382.     »Vce  cdso  Alcoholism 
Disseminated  sclerosis — 

absence  of  abdominal  reflexes  in, 
332 

ataxia  in,  272,  278 

clonus  in,  344 

emotional  state  in,  59 

erythromelalgia  a  symptom  in,  372 

motor  paraplegia  due  to,  321 

nystagnuis  in,  144 

optic  atrophy  in,  135,  139 

staccato  speech  in,  124 

transient  paralj^sis  in,  268 

vertigo  in,  169 

in  war,  512 
Disuse,  atrophy  fioni,  258,  409 
Dor.sal  longitudinal  bundle,  14 
Double  consciousness,  382,  401 
Drop-foot  and  drop-wrist  in  peripheral 

neuritis,  214,  243 
Drowsiness,  57,  455-457 

hypnotic,  457 

pathological,  455-457 
Dumbness — 

of  deaf-mutes,  126 

of  imbeciles,  126 
Dysnesthesiiie,  181 
Dysarthria,  119,  122.    See  also  Articnla- 

tion — defects 
Dysbasia  angio-scierotica,  263 
Dysdiadochokinesia,  277,  479 
Dysphagia,  hysterical,  411 
Dyspituitarism,  476 
Dystrophy,  muscular.     See  Myopathy 

E. 

Ear,  auditoi-y  fibres  of,  47 

disorders — gait  in,  299  ;  herpes  of 
external  auditory  canal,  157,  164, 
311  ;  otitis  media.  See  that  title  ; 
tinnitus  from,  157  ;  vertigo  from, 
169,  170 

inner,  afferent  impulses  from  semi- 
circular canals,  167 


568 


NEEVOUS  DISEASES 


Echolalia,  101 
Ectopia  pupillae,  137 
Electricity — 

abnormal  reactions,  424-427 

condenser  reaction,  425 

faradic  reactions,  421 

galvanic  reactions,  422 

polar  galvanic  reactions,  422 

reactions  of  degeneration,  426 
Electro-diagnosis,  415-427 

prognosis,  427-428 
Elephantiasis  nervorum,  316 
Embolism,  cerebral,  48,  51,  109 
Encepho-malacia,  184 
Enophthalmos,  59,  360,  362,  364 
Enteric    fever,    absence    of    abdominal 

reflex   in,    332;    "coma-vigil"   of, 

72  ;  headache  of,  184 
Enm'esis,  348 
Eosinopliilia    of    cerebro-spinal     fluid, 

169 
Epicritic  cutaneous  sensibility,  16  ;  loss 
of,   213 ;    recovery   of,    242  ;   test  of, 
199 
Epigastric  reflex,  331 
Epilepsy,  75  ct  seq. 

bilateral  excision  of  cervical  sym- 
pathetic for,  365 

chronic,  posture  and  gait  in,  303 

distinguished  from  hysteria,  75  et 
seq.  ;  and  Meniere's  disease,  171 

Jacksouian,    74,    80-82,    203,    466- 
469 

major,  or  "grand  mal,"  76 

masked,  or  larval,  78 

minor,  or  "petit  mal,"  77,  267 

post  -  epileptic     automatism,      78  ; 
coma,  71 

premonitory  symptoms,  75 

sudden  falling,  267 

in  war,  512 
Epileptiform  fits,  71,  79 

in  alcoholics,  79 

aphasia  following,  109 

in  asphyxia,  79 

in  cerebellar  disease,  86,  480 

cerebral,  classification  of,  74 

deep  reflexes,  abolition  of,  342 

in  general  paralysis  of  insane,  79 

headache  following,  185 

infantile,  82 


Epileptiform  fits  {continued) — 

in  intra-cranial  tumours,   80,  466- 
469 

Jacksonian.     See  Epilepsy 

myoclonus  allied  with,  90 

in  psychasthenia,  79 

sensory,  81 

in     Stokes- Adams    syndrome,    71, 
83 

toxic,  79 

vertigo,  an  aura  of,  169  . 

Epistaxis,  52,  184 
Equilibration — 

afferent  fibres  for,  20 

centre  for,  28,  167 

nerve  of,  164 
Erb— 

juvenile  atrophic  myopathy,  255 

motor  points,  416,  417,  421 

tetany,  sign  of,  85 
Ereuthophobia,  383 
Erythromelalgia,  59,  195,  197,  372 
Eulenberg's  disease  (Paramyotonia  con- 
genita), 262 
Eunuchism,  pituitary,  476 
Eustachian    tube,    obstruction    causing 

vertigo,  167 
Exophthalmic  goitre — ■ 

alopecia  in,  319 

blood-changes  in,  367 

cramp  in,  267 

cutaneous  pigmentation  in,  369 

dermographism  in,  375 

von  Graefe's  sign  of,  366 

intestinal  symptoms,  369 

Mcebius's  sign,  146 

stimulation  of  sympathetic,  symp- 
toms due  to,  367 

tremor  in,  92 

tremulous  respiration  in,  92 
Exophthalmos,  59,  238,  366 
Eye,  muscles  of — 

innervation  of,  135 

paralysis   of,   47,   54,   95,   140-151, 
225,  476 
Eyebrow  in  Third  nerve  paralysis  and 

hysterical  ptosis,  144 
Eyes,  "conjugate  deviation"  of,  9,  98, 
148,  295,  469 

See  also  umler  Optic,  Pupils,  and 
Vision 


INDEX 


569 


F. 
Facial  amestliesia,  lesions  causing,  17, 

153 
Facial    honii-atiuphy,   progressive,   156, 

321 
Facial  hemi-s[«asni,  102,  103,  162 
Facial  motor  points  (Erb's  diagram),  -llti 
Facial  muscles,  innervation  of,  157-161 
Facial  ]ialsy,  158-163 

artiuulative  difficulty  in,  120 

auditory  nerve  disease  accompany- 
ing, 166 

contracture  secondary  to,  162 

lesion  of  Sixth  nucleus,  associated 
with,  149,  162 
Facio-scapulohumeral    myopathy,    121, 

250,  254,  256 
Fieces,  incontinence  of,  349 
Fallopian  aqueduct,  153,  157,  160 
Family  gangrene,  373 

history  in  nervous  diseases,  56 

progressive    hypertrophic    neuritis, 
238 

periodic   paralysis,    266,    341,    373, 
424 
Faradic  electricity,  415  ct  seq. 

reactions,  421 
Fatigue — 

temporary  ataxia  due  to,  278 

tremor  of  muscular,  92 
Fevers,  bladder  trouble  in,  348 
Fibrillary  movements,  58,  89 
Fillet,  47 ;   degeneration,   36 ;   superior 

decussation  of,  20 
Fissured  fractures  of  cranium,  489 
Fissures — 

calcarine,  45 

lesions,  126,  442-443 

parieto-occipital,  42 

Rolaudic,  4,  5,  6,  17,  20 

Sylvian,  4,  6,  20,  47 
Fits,  74-87 

cerebellar,  86,  480 

cerebral,  74 

classification,  74 

cortical  lesions  and,  80-82 

epileptiform.     See  that  title 

hysterical.     See  under  Hysteria 

infantile,  82 

Jacksonian.     See  that  title 

scheme  of  investigation,  75 


Fits  (coiUinued) — 

strychnine  causing,  84 

in  sub-cortical  tumours,  80,  82 
Flaccid  paralysis,  35,  222,  232-247.  405 
Flechsig's  auditory  gyrus,  47 
Focal  signs  of  brain  injuries,  499-572 
"  Folic  dc  pourijuoi,"  383 
Foramen — 

of  Key  and  Retzius,  433 

ofMagendie,  433 
Forced  rotatory  movements,  479 
Fore  arm  sign  of  Leri,  410 
Formatio  reticularis,  lesions  of,  17 
Formication,  58 
Fractures  of  cranium,  varieties  of,  489 

depressed,  tits  due  to,  81 
Fragilitas  ossium,  322 
Freud's  views  on  hysteria,  384-386 
Friedreich's  ataxia,  99,  273-274 

articulation  in,  122 

deep  reflexes,  loss  in,  274,  341 

gait  in,  298 

Marie's  ataxia  compared  with,  276 

nystagmus  in,  144 

sensory  changes  in,  273 

spontaneous  movements  in,  99 

tabes  distinguished  from,  "273 
Frohlich's  syndrome,  476 
Frontal  region,  wounds  of,  508,  509 
Functional  and  Organic  disease,    lioun- 

dary  line  between,  60,  61,  378,  413 
Fundus,  ocular,  pathological  conditions 

of,  134,  135 

G. 
Gait,  293-303 
ataxic,  298 

cerebellar,  263,  276,  299 
in  chorea,  302 
of  chronic  epilepsy,  303 
in  cysticercus  of  Fourth  Ventricle, 

169 
in  deformities,  303 
high-stepping,  300 
hysterical,  296,  407-409 
in  lacunar  hemiplegia,  68,  296 
of  paralysis  agitans,  302 
in  peripheral  neuritis,  301 
reeling  or  titubating,  299 
"scissor,"  296 
side  (Flankengang),  297 


570 


NERVOUS  DISEASES 


Gait  [continued) — 

spastic,  294 

testing  mode  of,  293 
Ganglia.    Sec  Ciliary,  Gasseiian,  Genicu- 
late, etc. 
Gangrene — 

family,  373 

symmetrical   of  Raynaud's  disease^ 
313,  371 
Gasserian  ganglion,  137,  138,  152,  153, 

156,  358  ;  inflammation,  311 
General  paralysis  of  insane — 

Argyll-Eobertson    phenomenon    in, 
136,  139 

articulation  of,  122 

cerebral  lifemorrhage  in,  65 

cerebro-spinal    fluid   in,    267,    441- 
444 

deep  reflexes,  loss  in,  341 

epileptiform  fits  in,  79 

hemiplegia  in,  265,  266 

pachymeningitis   hemorrhagica  in, 
67 

pupils  in,  136,  139 

tremors,  spontaueous  in,  99,  122 

in  war,  512 
Geniculate  ganglion,  152,  157,  160,   161, 
164 

inflammation  of,  157,  164,  311 
Genital  reflex,  346 
Genu  recurvatum,  291  :  fig.,  290 
Giddiness,   147,   162,  167  ct  seq.,   183, 
445,  463,  465 

See  also  under  Vertigo. 
Gigantism,  306,  476 

Glaucoma,  excision  of  cervacal    sympa- 
thetic for,  365 
Gliomata,  484 
Globulin  in  cerebro-spinal  fluid,  tests  for, 

435 
Globus  hystericus,  75,  84,  400,  411 
Glosso  -  labial    hemi  -  spasm,    289,     290, 

407 
Glossy  skin,  58,  309 
Gluteal  reflex,  331 
Glycosuria,  169,  307,  369,  478,  483 
Gold  reaction,  colloidal,  436-438 
Goldflam's  sign  of  intermittent  claudica- 
tion, 264 
Gordon's  paradoxical  flexor  reflex,  334 
Gowers'  tract,  diagram,  etc.,  17,  18 


Grasset  and  Gaussel's  test,  222 
Graves'  disease.  *S'ce  Exophthalmic  Goitre 
Gumma,  intra-cranial,  188,  483 
fits  from,  80 

headache  due  to,  183,  185 
neuralgia  due  to,  188 
Gustatory  path,  47,  152  ;  diagram,  152 
Gutter  fractures  of  cranium,  489 
Gyrus,  angular — 

arterial  supply,  51 
cortical  lesion,  132,  471 
visual  word  centre,  46,  107,  113 
auditory  (Flechsig's),  47 
Heschl's,  47,  107 

tumours  of,  471 
lingual,  45 

uncinate,  lesions  of — 
fits  due  to,  81 

olfactory   centre,    44,    470  ;    dis- 
orders of,  128 
tumours  of,  470 

H. 

Habit  spasms,  100,  103,  403,  413 
Hsematomyelia,  from  wounds,  515 
Hasmoglobinuria,  paroxysmal,  372 
Hasmophilia,   cerebral    hsemorrhage   in, 

65 
Haemorrhage,  cerebral — 

aphasia  from,  109 

artery  of  (diagram),  49 

at  birth,  83 

blood  pressure  in,  64 

cerebro-spinal  fluid  in,  434 

in  children,  65 

chronic-subdural,  66 

coma  in,  63 

fits  due  to,  81 

in  general  paralysis  of  insane,  65 

headache  preceding,  184 

Meniere's  disease  distinguished  from, 
171 

pontine,  67 

spontaneous,  63-65 

subarachnoid,    cerebro-spinal    fluid 
in,  433 

subdural,  chronic,  66,  67 

traumatic,  493 

trophic  changes  in  nails  in,  320 

vertigo  from,  169 


INDEX 


571 


Hair — 

blanching  of,  If.O,  HI 8 

falling  of,  320 

in  progressivo  facial  atrojiliy,  If)*! 

trophic  changes,  318-320 
Half-vision  centres,  45,  4G,  472-473 
Hallucinations — 

auditory,  166 

olfactory,  128 

pain,   hysterical   hallucinations    of, 
389 

visual,  81,  473 
Hand,  deformities  of,  283-284 
Haphalgesia,  400 
Head  injuries,  coma  in,  62,  65 
Head,  wounds  of,  489-491 
Headaches,  182-187 

angio-neurotic,  186 

clavus  hystericus,  186 

gastric,  184 

of  gross  intra-crauial  disease,    183, 
403 

hysterical,  186,  389 

local  (extra-  and  intracranial),   1S2 

in  Meniere's  disease,  171 

migrainous,  186 

neurasthenic,  185 

post-epileptic,  185 

reflex,  184 

in  sunstroke,  185 

toxic,  184 

due  to  tumours  of  brain,  463 

unilateral,  185 
Head-rolling,  94 
Hearing.      See  under  Auditory 
Hemeralopia,   130 
Hemi-achromatopsia,  132 
Hemi-ansesthesia,  206  209 

crossed,  11,  21,  203,  204,  210 

hysterical,  segmental  type,  206,  392- 
397 

organic,  206-209 

cortical   and  sub-cortical,  208 

468 
lesions  causing    (diagram),    19, 

21,  208,  474 
sub-thalamic,  209 
thalamic,  95,  208,  474 
Hemianopia — 

bi-temporal   in   pituitary   tumours, 
478     • 


Hemianopia  {continuecJ) — 

definitions  and  cause,  132-134 

diagrams,  46,  133 

lesions  jjroducing,   10,  45,  132-134, 

472-473 
quadrantic,  45,  46,  134 
sub -cortical    word-liliiidness    asso- 
ciated with, 113 
varieties  of,  132-134 
Wernicke's    pupillary    reaction     in 
139,  473 
Hemi-atrophj',  facial,  156,  321 
Hemicrania,  hysterical,  389 

See  Migraine 
Hemi-hyperffisthesia,     hysterical,    390  ; 

thalamic,  204 
Hemi-hypertrophy,    facial    (fig.),    321  ; 

universal  (fig. ),  308 
Hemiopic     pupillary     reaction,      Wer- 
nicke's, 139,  473 
Hemi -paraplegia,  57 
Hemiplegia — ■ 

alternate,  218,  482 

angio-spastic,  265 

aphasia  in,  109,  122 

apraxia  in,  116-118 

articulation  after,  122 

ataxia,  associated  with,  278 

athetosis  following,  96  ;  fig.,  97 

bed-sores  in,  311-312 

bilateral,  123,  218 

bone-changes  in,  321-322 

capsular  lesion  causing,  9-10 

chronic,  322-325 

combined  flexion  of  liip  and  trunk, 

220  ;  fig.,  221 
crossed,  252,  482 
definition  and  forms  of,  2]  8 
dolorosa,  182 
gait  in,  294-295 
in  general  paralysis,  266 
Grasset  and  Gaussel's  sign  of,  220 
headache  preceding,  184 
in  head  injury,  65 
hysterical    (functional),    220,    287- 
290,  297 
absence  of  plantar  reflexes,  335 
anosmia  in,  128 
Leri's  forea,rm  sign  in,  410 
infantile,  321  ;  figs.,  285,  322 
ipso-lateral,  22.5 


572 


NERVOUS  DISEASES 


Hemiplegia  (continued)— 

joint  affections  in  chronic,  327 

lacunar,  68,  296 

lesions   causing,  diagnosis,   68,    95, 
434,  465 

ligature  of  carotid  artery  after,  512- 
514 

loss  of  certain  reflexes  in,  334-336 

muscular  wasting  in,  259 

pandiculation  in,  98 

posture  in,  287 

synkinesia  in,  98 

thrombosis  causing,  in  war,  514 

transient,  265,  266 

tumours  causing,  467  et  seq. 

visual  fields  in  cases  of  (diagram), 
398 
Hemispasm,  facial,  102-103 
Hereditary  ataxia,  Friedreich's,  99,  273- 

274  ;  Marie's,  276 
Hernia  cerebri,  497-498 
Herpes,  facial,  157,  164,  311 
Herpes  zoster,  181,  189,  206,  311,  318 
Heschl's  gyrus,  47,  107 

tumours  of,  471 
Hiccough  in  intra-cranial  disease,  465 
Hippus,  138 

Holmgren's  tests  for  colour  vision,  130 
Hunger,  cortical  centre  for,  48 
Huntington's  chorea,  96 
Hydrarthrosis,  intermittent,  375 
Hydrophobia,  84  ;  hysterical,  84 
Hyoscine  chorea,  96 
Hyperacousis,  160 

Hyperemia,  cerebral,  167,  168,  183,  186 
Hypersesthesia,  204-206 

hysterical,  areas  of,  197,  205,  390 

mapping  out  areas  of,  200 
Hyperalgesia,  206,  390 
Hyperidrosis,  localised,  375 
Hyperkeratosis,  in  nerve  lesions,  534 
Hypermetria,  cerebellar,  277 
Hypermetropia,  headache  from,  184 
Hyper-pyrexia,  64,  68,  185 
Hyper-thyroidism,  319 
Hyper- trichosis,  318 
Hypertrophic  progressive  neuritis,   237, 

274 
Hypertrophy  of  muscle,  212 
Hypnotic  suggestion,  73,  386 
Hypnotic  trance,  73,  386 


Hypo-sesthesia,  204 

Hypoglossal  nerve.     See  Cranial  Nerves 
Hypoglossal  nucleus,  157,  180 
Hypo-thyroidism,  320 
Hypotonia  of  muscles,  290-292 
choreic,  96 
tabetic    (diagrams    of   cases),   271, 

290.  291 
Hysteria,  383-414 

age  and  sex,  eff"ect  in,  75,  413 
allocheiria  in,  201,  204,  400 
alternating  personality,  382,  401 
ambulatory  automatism,  402 
anaesthesia.     See  2iiider  Antesthesia 
ankle-clonus,    spurious,    221,    343, 

409 
aphasia  and,  114 
articulation  in,  125,  389 
ataxia  in,  279 

bio-chemical  changes  underlying,  60 
Charcot's    "  grande   hysteric,"    76, 

401 
in  children,  408,  413 
combination  with   organic   disease, 

61 
concentric     contraction     of    visual 

field,  132,  397.  398 
contractures,  287-290 
cough  in,  413 

crossed  amblyopia  in,  45,  132 
dermographism  in,  413,  414 
double  consciousness  in,  382,  401 
fits  in — 

catalepsy,  77,  377 
classification,  74 
distinguished     from     epileptic 
fits,  76,  376 
following  electric  shocks,  404 
Freud's  views  on,  384-386 
gait  in,  296,  407-409 
glosso-labial  hemispasm,   289,   290, 

407 
hemiplegia,       distinguished      from 

organic,  220,  287-290 
hydrophobia  simulated,  84 
hypersesthetic  areas  in,    197,   205, 

390 
inhibition  deficient  in,  386 
joint  pains  in,  328,  389 
major,  74,  76,  401 
minor,  74,  76,  77 


INDEX 


573 


Hysteria  (continued) — 

motor  phenomena  in,  400-410 

muscular  wasting  in,  259 

neurotonic  reaction  in,  424 

organic  disease,  distinguished  from, 
60,  378,  413 

pains  of,  197 

paralysis.     See  itnder  Paralysis 

paraplegia,     simulating     injury    nf 
spinal  cord,  516 

plantar  reflex,  in  diagnosis  of,  334, 
335 

post-epileptic,  77,  400 

postures  in,  287-290 

psychical  synii)toms,  385-389 

psycho-analysis  in,  384 

ptosis,  144,  146 

reflexes  in,  77,  334,  335,  409-410 

sensory  symptoms  in,  385-400 

shell  amblyojiia  and,  399 

skin  affections  in,  413 

spasms  in,  104 

speech  defects  in,  388,  389 

trance  of,  72,  401 

transient  paralyses  in,  267 

vasomotor  phenomena  in,  410-412 

visceral  phenomena  in,  410-412 

war  neurosis  and,  73,  399 
Hysterofrenic   and    hysterogenic   areas, 

391 

I. 

Idiocy,  amaurotic  family,  135 
Idioglossa,  127 
Imperious  acts,  383 
Inco-ordination  (ataxia),  269-279 

articulative,  -122 

cerebellar,  30,  276,  277,  478,  479 

due  to  fatigue,  278 

hysterical,  279 

from  lesions  of  rubro-spinal  tract, 
279 

in  new-born  child,  269 

post-febrile,  278 

pre-  and  post-hemiplegic,  278 

in  progressive  hypertrophic  neuritis, 
274 

sensory  origin  of,  270 

tests  for,  269 

toxic,  278 
Jnfant,  new-born,  movements  of,  4 


Infantile  convulsions,  82 
Infantile  spinal  paralysis  (acute  anterior 
poliomyelitis),  232-234,  321 

cerebrospinal  fluid  in,  234 

lesions  causing,  40,  233,  234 

loss  of  deep  reflexes  in,  341 

tropic  changes  of  liones  in,  321 
Infantilism,  476-478 
Inguinal  region,  hysterical  tender  spots 

in,  390 
In  ion,  5 

Injuries,  spinal  symptoms  of,  20-21 
Insanity,  toxic  varieties  of,  58 
Insomnia,  458-461 

alcoholic,  460 

drugs,  use  of,  in,  459,  460 

emotional,  458 

extrinsic,  458 

and  insanity,  461 

intrinsic,  458 

primary  or  nervous,  460 

vascular  causes  of,  458 
Intermittent  arterial  claudication,  195, 
197,  263,  374 

Goldflam's  sign  in,  264 
Intermittent  hydrarthrosis,  375 

cerebral  claudication,  265 

spinal,  264 
Internal  capsule — 

anatomy,  7-10  ;  diagram,  9 

auditory  fibres  of,  47 

lesions  of,  9,  10,  148,  206,  224 

motor  fibres,  7 

sensory  fibres,  7-9 

tactile  fibres,  17 

visual  fibres,  10^  45 
"Interosseal  attitude""  (diagrams),  302. 

303 
Intervertebral  ganglion    (ganglion    cell 

of  posterior  root),  35,  311 
Intra-cranial  htemorrhage,  63-68 
Intra-cranial  pressure,  65,  80,  183 

lumbar  puncture  in  relief  of,  445 
Inversion  of  radial  reflex,  340 
Involuntary  movements,  88-105 

associated,  97 

athelotic,  96 

choreic,  96 

myokymia,  89 

reflex  spasms,  102-104 

rigors,  88 


574 


NERVOUS  DISEASES 


Involuntary  movements  (contrmied) — 

in  tabes,  99 

tremors,  92-94 
Ipso-lateral  pyramidal  tract,  11 
Irritation,  cerebral,  493 
Ischremic  myositis,  247 

from  injuries  of  arteries,  556 
Itching  sensation,  test  for,  200 


Jackson's  syndrome,  180 

Jacksonian  fits,  74,  80-82,  208,  466-469 

papillary,  469 
Jaw  reflex,  336 
"Jaw- winking,"  150-151 
Jendrassik's  reinforcement  of  knee-jerk, 

338,  339 
Jews,  amaurotic  family  idiocy  amongst, 

135 
Joints — 

hysterical  pains  in,  327,  389 
trophic  changes  in,  323-329 
Joint-sense,    198,   202,   271  ;    tests   for, 
202 

K. 

Keratitis,  bacillus  of,  156 

neuro-paralytic,  155 
Kernig's  sign   of  cerebro-spinal  menin- 
gitis, 68,  311,  442 
Kidney  disease — 

arterio-sclerosis  of  chronic,  vertigo 
in,  168 

cerebral  hfemorrhage  in,  64 

floating  kidney,  191 

uraemic  convulsions  of,  79,  446 
Kinesthetic  sense,    198,   202,  259  ;  test 

for,  202 
Kleptomania,  382 
Knee-clonus,  343 
Knee-jerk,  336-389 
Korsakow's  psychosis,  58 


Labyrinth,  disease  of,  164,  170,  171 

vertigo  of,  170-171 
Labyrinthitis,  143 
Lachrymal  secretion,  paralysis,  155 
Lactation,  tetany  during,  86 


Lacuna  hemiplegia,  68,  296 

Lalling,  126 

Landouzy-Dejerine  type   of  myopathy, 

121,  250,  254,  256 
Landry's  paralysis,  232,  244,  341,  439 
Lange's  colloidal  gold  reaction,  436-438 
Laryngismus  stridulus,  82,  85 
Larynx — 

ataxy  of,  122 
innervation  of,  174-177 
myoclonus  of,  89 
paralysis,  174-177 
Lasagne's  symptom,  407 
Lateral  sinus.     See  Sinus 
Laudanum  poisoning,  70 
Laufenauer's     method     of    reinforcing 

knee-jerk,  339 
Laugh,  spastic,  95 
Lead  poisoning — 

convulsions  in,  79 

lymphocytosis     of    cerebro  -  spinal 

fluid  in,  441 
optic  neuritis  in,  134 
palsy  in,  214,  243  ;  absence  of  sen- 
sory changes  in,  214,  232 
tremor  of,  92 
visceral  symptoms,  369 
Leg,  sensory  fibres  from,  20 
Lenticular  degeneration,  progressive,  95 
hepatic  cirrhosis  with,  96 
tremors  in,  95 
Lenticular  zone,  lesions  of,  115 
Lentieulo-striate  artery,  51 
Leprosy,   arthropathies  of,   323  ;   leuco- 
dermia    in,    315 ;    maculo-ansesthetie 
type,  214,  315  ;  neuritis  of,  214,  310 
Lepto-meningitis,    localised,     compared 

with  spinal  tumours,  228 
Leri's  forearm  sign,  410 
Leucocytosis  of  cerebro-spinal  fluid,  440- 

444 
Leucoderma,  314 
Leukieraia,   65  ;  cerebro-spinal  fluid  in, 

441       . 
Levator   palpebrte    superioris,    innerva- 
tion, 135,  358  (diagram)  ;  paralysis  of, 
144,  150,  158,  360 
Light  reflex.     See  binder  Reflexes 
Limp,  intermittent.     See  Claudication 
Lypo-dystrophy,  progressive  descending, 
318 


INDEX 


575 


Lips,  paralysis  of,  180 

Lisping,  126 

Localisation,  cerebral,  4-11 

Lock-jaw.     Sec  Tetanus 

Locomotor  ataxia.     Sec  Tabes 

Longitudinal  sinus,  su[ierior,  tlironibosia 
of,  52 

Lordosis  (with  figs.),  252 

Luetin  reaction,  483 

Lumbago,  192,  247 

Lumbar  puncture.     Sec  Thecal  puncture 

Lunibo-abdominal  neuralgia,  192 

Lumbo-sacral  cord — 

disease  symptoms  in,  187 
muscular  localisation  in  (diagram), 
41 

Lumbo-sacral  plexus  and  branches,  30, 
38  ;  wounds  of,  554-555 

Lymphocytosis  of  cerubro-spiual  Huid, 
79,  189,  267,  311,  440-444  ;  diag- 
nostic significance.  442-443 


M. 

Macuogenito.somia,  475 

Macropsia,  400 

Main  de  predicateur,  284 

Main  de  singe,  283 

Main  en  griffe,  283 

Malarial  coma,  72 

Malingering,  Mannkopf's  sign  in,  390 

Mammary  neuralgia,  1 90,  390 

Mannkopf's  sign  of  real  hyperajsthesia, 

390 
Marie's  hereditary  cerebellar  ataxia,  276 
Masked  epilepsy,  78 
Mastodynia,  190 
Meckel's  ganglion,  151,  152 
Median  nerve,  wounds  of,  533 
Medulla — 

auditory  fibres  in,  47 

cranial  nerves  (diagram),  129,  130 

lesions  of,    11,  209,  225,    274  276, 
358,  483 

Meniere's  disease,  implicated  in,  170 

pupil-dilating  centre  in,  357 

respiratory  centre  in,  4 

sensory  fibres,   course  of,   18  ;   dia- 
gram, S 

stimulation  of  nuclei  in,  1 


Melancholic  anergia  distinguished  from 

psychasthenia,  381 
Memory,  loss  of,  58,  62  ;   postepileptic 

loss  of,  78 
Meniere's  disease  (labyrinthine  vertigo), 

170-171 
Meningeal  adhesions,  in  brain  wounds, 

493 
Meninges — 

cerebral,  convulsions  from  hicmor- 

rhage  into,  83 
pain,  sensitiveness  to,  181 
s[)inal,  diseases  of,  196 

root  i)ains  of,  188,  1S9,  196 
Meningism,  442,  514 
Meningitis  — 

basal,  69,  163,  18S 
in  brain  wounds,  497 
cerebro-spiual  Huid  in,  69,  434-442 
tits  due  to,  83 
fluid  pressure  in,  433 
headache  in,  185 
lepto,  circumscribed  spinal,  228 
lumbar  puncture  for,  444,  445 
meningococcal,  438,  441,  514 
septic  cerebro  spinal,  312,  435,  440 
serous,  486 

spinal,  root  pains  in,  196 
syphilitic  basal,  163,  188 
tuberculous,  183.  441,444 
Meningomyelitis,  traumatic,  516 
Menstrual   periods,    headaches    during, 

183 
Meralgia  paraesthetica,  194 
Mercury  poisoning,  tremor  of,  92 
Metameric  and  root  distribution  of  sen- 
sory and  motor  fibres,  38 
Meteorisra,  369,  374 
iNfeynert's  fibres,  136 
Micropsia,  400 
Micturition,  347  ;  centres  for,  347-348  ; 

in  hysteria,  410,  412 
Middle  ear — 

disease  of,  162,  165,  170 
innervation,  152 
Migraine,  186  ;   ophtalmopl<^gique,  150, 

187 
Millard-Gubler  syndrome,  11.  226 
Miners'  nystagmus,  144 
Mtcbius's  sign  iu  exophthalmic  goitre, 
146 


576 


NERVOUS  DISEASES 


Moles,  hairy,  318 

MoUuscum  fibrosuin,  ?17 

Monakow's    bundle  (riibro-spinal),    12 ; 

lesions  in,  149,  279,  341,  475 
"Monkey-hand,"  283 
Monoculai'  diplopia,  400 
Monophobia,  383 
Monoplegia,  7,  224,  499  ;  hysterical,  403- 

405 
Morvan's  disease,  211,  310 
Motor  aphasia,  108,  114-116,  469 
Motor  areas,  localisation  of,  5-6 
Motor  centres  in  cerebellar  cortex,  29 
Motor  cortex,  lesions  of,  7,  467-468,  498- 

502 
Motor  nerves — 

fibrillary  tremors  in  paralysis  of,  89 
regeneration  of  fibres,  242 
Motor  neurones,    upper  and   lower,  34, 

222 
Motor  paralyses,  215-259 

functional  or  organic,  219 
lower   neurone  type,    35,   232-259  ^ 
distinguished     from     upper 
neurone  type,  222 
distinction     between     anterior 
cornual      and      nerve  -  root 
lesions,  232-233 
Landry's   paralysis,    232,    244, 

341 
level   of   lesion,    diagnosis    of, 

232 
from    multiple    peripheral    le- 
sions, 238-239,  242-243 
muscles,  affections  within,  247 
plantar  reflex  in,  222,  334 
sensory  phenomena  in,  222 
recurrent  and  transient,  260-268 
Eulenberg's  disease,  262 
family  periodic  paralysis,  266 
in  general  paralysis  of  insane, 

266 
in  hysteria,  267 
intermittent  arterial   claudica- 
tion, 263 
intermittent     spinal    claudica- 
tion, 264 
in  minor  epilepsy,  267 
myasthenia  gravis,  260 
myotonia  atrophica,  263 
occupation  neuroses,  265 


Motor  paralyses  {continued) — 

recurrent  and  transient  [contiyiued  — 
sign  of  disseminated  sclerosis, 

268 
in  tabes,  267] 
tetany,  267 

Thomsen's  disease,  262 

upper  neurone   type,    35,  222-231  ; 

bilateral,  226  ;  distinguished 

from    lower    neurone    type, 

221-222 

exaggeration  of  deep  reflexes  in, 

342 
flexed  and  extended  types  of, 

285-286 
level   of   lesion,    diagnosis   of, 

224-231 
unilateral,  224-226 
Motor  points,  421  ;  diagrams,  416-422 
Mucuna  pruriens,  200 
Miiller,  non-stiuated  muscle  of,  paralysis 

357 
Mumps,  lymphocytosis  of  cerebro-spinal 

fluid  in,  441 
Muscles,  atrophy  of — 

causation,  35,  232,  234,  304 
fibrillary  tremors  in,  89 
in  hemiplegic  arthritis,  327 
in  hysteria,  403 
idiopathic.     Sec  Myopathy 
in  neuritis,  238 

peroneal  type.  Tooth's,  236-237 
pi'ogressive    (chronic    anterior 
poliomyelitis),    89,    234-235, 
341,  427 
dystrophy  of.     See  Myopathy 
electrical  reactions,  420-427 
fatigue  -  paralysis,    in    myasthenia 

gravis,  121 
hypotonia,  271,  290-293 
motor  points,  Erb's  diagrams,  416- 

422 
non- striated    involuntary,   reflexes 

of,  330,  346 
sensation,  active,  202 
sensibility  to  pressure,  202 
sensory  fibres  from,  19 
testing,  in  motor  paralysis,  217 
Muscle-spindle,  a  trophic  centre,  35 
Muscular  analgesia  in  tabes,  203 
Muscular  cramp,  267 


INDEX 


577 


Muscular  localisation  iu  cervical  enlarge- 
ment, 41 

in  lurabo-sacral  cord,  41 
"Muscular  sense,"  definition,  202 
Musculo-spiral   nerve,  ^laralysis  of,  61, 

268-284,  536 
Mutism,  hysterical,  73,  125,  388 
Myalgia,  192 
Myasthenia  gravis,  121,   130,  144,  260, 

424 
Myasthenic  reaction,  424 
Myatonia  congenita,  2111 
Mydriasis,  137 
Myelitis,  60,  231,  312-313 
Myclo-malacia,  due  to  wounds,  515,  522 
Myoclonous,  89-91 

nystagmus,  91,  144 
Myoclonus  cpilepticus  (Uuverricht's),  90 
Myoidema,  217 
Myokymia,  89 
Myopathy — 

atrophic  type,  254-258 

atrophy  of   nuclear   origin   distin- 
guished from,  249 

Erb's  juvenile  type,  255 

facio-scapulo-humeral  type,  121, 163, 
250,  256 

gait  and  posture  in ,  300 

pseudo-hypertrophic  type,  251  254 
Myosis,  137,  359 
Myositis,  147,  202,  247 

ischsemic,  247 
Myotomes,  38 
Myotonia  atrophica,  263 
Myotonia  congenita  (Thomsen's  disease), 

262,  425 
Myotonic  reaction,  262,  425 
Myxcedema  and  drowsiness,  455 


N. 

Njevi,  cutaneous,  315-316 

Nails,  trophic  changes,  320 

Narcolepsy,  72,  457 

"Narcosis,  traumatic,"  62 

Nasal  crises,  129 

Nausea.     See  wider  Vomiting 

Neck,  motor  points  (Erb's  diagram),  416 

Nephritis — 

optic  neuritis  in,  134 
uraemic  fits  of,  71,  79,  446 


"Nerve  deafness,"  166 
Nerve  plexus.     Hcc  Plexuses 
Nerve  roots.     See  Spinal  Nerves 
Nerves.       See    under    Ciauial,    Motor, 
Peripheral,  Spinal,  also  names  of  par- 
ticular nerves 
Nervous  system,  anatomy  and   physio- 
logy of,  1-55 

scheme  for  routiac  examination  of, 
57-59 
Neuralgia — 

blanching  of  hair  iu,  CIS 

brachial,  192-193 

coccygodynia,  192 

hyperotsthesia  in.  205-206 

mammary,  190,  i>89 

mcralgia  pantsthetica,  194 

phrenic,  190 

post-herpctic,  311 

sciatic,  193,  335 

"tender  points,"'  187,  19£ 

trigeminal,  187 
Neurasthenia — 

causes  and  diagnosis,  379-381 

deep  reflexes  exaggerated  in,  342 

distinguished  from  hysteria,  379 

headaches  associated  with,  185 

mydriasis  in,  137 

toxic,  379 

traumatic,  189 
Neuritis — 

alcoholic,  59,    206  ;    figure  of  case, 
244 

arsenical,  317,  320 

diabetic,     perforating     ulcers     in, 
310 

glossy  skin  in,  309 

lead,  243-244 

leprous,  214,  310 

loss  of  deep  reflexes  in,  341 

multiple  or  peripheral,  59,  196,  202, 
206,  213-214,  300,  320,  345 

optic.     See  that  title 

post-diphtheritic,  120,  140,  163 

progressive,      hypertrophic,      237, 
274 

retro-bulbar,  135 

sciatic,  194 

following  wounds,  539 
Neuro-fibromata,  197,  316 
Neuromimesis,  378 


578 


NERVOUS  DISEASES 


Neurones — 

cerebello-dentate,  36 

cortico-bulbar,  120,  122 

dentato-tlialaniic,  36 

lower  motor  (spino-muscnlar),  54  ; 
lesions  of,  35,  222.  See  also 
Motor  Paralysis,  Lower  Neurone 
type 

sensory,  lesions  of,  35 

spino-cerebellar,  36 

thalamo-cortical,  36 

upper    motor   (cortico-spinal),    34  ; 
lesions  of,  35,  224.    See  also  Motor 
Paralysis,  Upper  Neurone  type 
Neuroses — 

hysteria,  383-414 

neurasthenia,  379-381 

j)sychasthcnia,  381-383 
Nicotine  poisoning,  tremors  of,  92 

See  also  Tobacco 
Nightmares,  457 
Noguchi's  test  for  globulin,  435 
Nuclear  ophthalmoplegia,  148-149 
Nuclei — 

ambiguus,  172 

auditory,  47,  166 

bulbar,  121 

caudate,  7,  50 

cerebellar,  25,  26,  28 

cuneate,  16,  19 

Deiters',  25,  26,  28 

dentate,  25.  26 

Edinger-Westphal,  136 

emboliformes,  25,  26 

globosi,  25,  26 

glosso-pharyngeal,  164 

gracile,  16,  19 

hypoglossal,  157,  180 

lenticular,  7  ;  lesions,  95,  123 

medullary,  16,  120 

ocular,  25,  30,  95,  136 

red  (diagram),  27  ;  lesions,  95,  149, 
225,  279,  475 

Sixth  cranial  nerve,  11,  149 
Nyctalopia,  130 
Nystagmus,  142-144 

cerebellar,  30 

in  disseminated  sclerosis,  144 

facial,  99 

fistular,  143 

in  Friedreich's  ataxia,  144,  274 


Nystagmus  {continued)  — 

labyrinthine  or  vestibular,  142, 143 

miners',  144 

myoclonus,  91,  144 

pendular,  142 

reflex  (optic,  vestibular),  148 

rhythmic,  142 

thermic,  143 

vestibular,  142 


o. 

Obsessions  of  psychasthenia,  382 

Occipital  region,  wounds  of,  506-508 

Occupation  neuroses,  102,  265,  278 

Ocular  headaches,  184 

Ocular  paralysis.     See  under  Paralysis 

Ocular  symptoms  in  Raynaud's  disease, 
372 

Ocular  vertigo,  170 

Oculo-cardiac  reflex,  346 

Oculo -motor  (Third)  nerve.  Sec  under 
Cranial,  nerves 

Oculopupillary  fibres  of  cervical  sym- 
pathetic, 357 ;  paralysis  of,  359-360  ; 
diagram,  358 

(Edema,  acute  angio-neurotic,  374 
blue  hysterical,  413 
cerebral,  traumatic,  496 
spinal,  traumatic,  526-528 

(Esophagus,  hysterical  spasm  of,  411 

Olfactory  nerves,  128  ;  path,  44 

Olivary  body,  17,  26 

Olivo-ponto-cerebellar  atrophy,  276 

Ophthalmoplegia,  136 

nuclear  (internal,    external,  total), 
149 

Opisthotonos,  76,  530 

Opium  poisoning,  coma  of,  70  • 

Oppenheim's  reflex,  334 

Optic  atrophy,  132,  135,  137,  139,  478 

Optic  chiasma — 

course  of  visual  fibres  in,  45 ;  dia- 
grams, 46,  134 
lesions  at  or  behind,  132-134,  139, 
478 

Optic  nerve,  45,  129 

Optic  neuritis,  134 

in  brain  wounds,  498 

in  diagnosis  of  coma,  63,  69 

headaches  with,  diagnosis,  183 


INDEX 


579 


Optic  neuritis  (roufhuinl)  — 

of  intra-cranial  tiuuoiii',  403 
lumbar  puncture  to  relieve,  44r) 
Optic  radiation,  45 
Optic  thalamus — 

centres  for  pleasure  and  pain  in,  20 
ceaties  for  visceral  sensations,  20 
lesions  of,  95,  182,  208,  225,  473 
micturition  centres  in,  348 
reflex  centre  of  emotion,  474 
sensory  fibres  of,  20,  474 
redistribution  in,  20 
visual  fibres  in,  45 
Orbicularis  oculi  (palpebrarum),  homolo- 
gous with  branchial  arch  of  fish,  151  ; 
innervation,  150 
Orbital  muscle  of  Miiller,  357  ;  diagram, 

358 
Orthostatic  albumimiria,  369 
"Osseous  sense,"  203 
Otic  ganglion,  157  ;  diagram,  152 
Otitis  media,  165-166 
vertigo  from,  170 
Ovarian  disease,  headache  from,  184 
"  Ovarian  tenderness,"  390 


Pachymeningitis,      interna      hremor- 
rhagica,  67 

spinal,  231 
Pain — 

course  of  fibres  subserving,  16-20 

headache,  182-187 

hysterical,  197,  389 

in  limbs,  192  ;  bilateral.  195 

loss    of    sense    of,    22,     200,    212- 
213 

paroxysmal  spontaneous,  195,  197 

reflected,  190 

root,  196 

tests  for  sense  of,  200 

in  trigeminal  area,  187-188 

in  trunk,  180-184 
Palate,  soft — 

hemi-atrophy,  156 

innervation,  153,  173 

paralysis,  bilateral,  120  ;  unilateral, 
172,  180 

reflex  movement,  317 
Palkesthesia,  203 
Palsies.     See  Paralysis 


Panatroplij',  loi.'al,  318 
Pandiculation,  93 
Paracousis,  160 
Par.-esthesia  200 

hysterical,  400 
Paradoxical  flexor  reflex,  334  ;  pupillary 

reaction,  140 
Paragraphia,  113 
Paral3'sis — 

alcoholic,  163,  214,  243 

alternats.     See  Grossed 

Brown  Sequard,  21,  203,  210,  228 

bulbar.     See  that  title 

of  cervical  sympathetic,  358-366 

cranial  nerves,  128-180 

crossed,  11,  61,  218,  225,  482 

facial,  120,  157-163,  225  ;   bilateral, 

163,  165 
family  periodic,  266,  341,  373,  424 
Fifth  nerve,  151-156 
glosso-labio-laryngeal.     See  Bulbar 

Palsy 
glosso-pharyngeal,  172 
hypoglossal,  120,  178-179 
hysterical,  267,  287-290,    403-408  ; 
figures,  288,  289,  296,  297,  387- 
388,  393-397,  404-408 
infantile,  233-234,  303,  321 
ischemic,  247-248 
Landry's,  232,  244,  341 
laryngeal,    organic   and    functional 

(diagrams),  173-176 
motor.     See  Motor  Paralyses 
motor  and  sensory  combined,  227, 

239 
musculo- spiral,  283 
myasthenia  gravis.     See  that  title 
ocular,  rheumatic,  147 
infra-nuclear,  149 
from     lesions     of     individual 

nerves,  141,  144-150 
nuclear  lesions,  149 
sirpra-nuclear,  148 
oculo-motor,  144,  145 
palatal,  106,  120,  172-174 
peripheral     motor     nerve     lesions, 

electro-prognosis  of,  427 
post-diphtheritic,  106,  120,  163 
spastic,  "  flexed  "  and  "extended  " 

types,  285-287 
tumours  in  cei'ebral.  468 


580 


NERVOUS  DISEASES 


Paralysis  agitans — 

articulative  difficulties  in,  124 
diagrams  of  cases,  94,  302,  303 
Parkinsonian  mask,  124,  302 
posture  and  gait  of,  302 
rigidity  of,  93 
tremor,  93 
in  war,  512 
Paramyoclonus  multiplex  (Friedreich's), 

89-91 
Para,myotonia     congenita     (Eulenberg's 

disease),  262 
Paraphasia,  112 
Paraplegia — 

bed  sores  in,  311 

brachial  and  crural,  218 

chronic,   trophic  changes  in   nails, 

320 
gait,  296 

hysterical.  288,  297,  387  (figs.) 
simulating  wounds  of   spinal  cord, 

516 
spastic,    61,   224,    227,    272,    294 ; 
flexed  and  extended  types  of,  285- 
287 
Paraplegia  dolorosa,  196 
Para-sympathetic  fibres,  351 
Parathyroids,    tetany   from   extirpation 

of,  85 
Parietal  region,  wounds  of,  510,  511 
Parkinsonian  mask,  124,  302 
Parosmia,  128 

paroxysmal,  129 
Penetrating  wounds  of  head,  490 
Penis,  analgesia  of,  in  tabes,  212 
Perforating  wounds  of  head,  490 
Pericarditis,  reflected  pain  in,  190 
Periostitis  of  skull,  183 
Peripheral  nerves — 

cutaneous  areas,  39 
lesions — 

anaesthesia,  213 
ataxia,  271 
mixed,  239-242 
motor     paralysis,     218,     233, 
427 
paths,  of  sensation  in,  14-16 
wounds  of — 

compression,  537 
concussion,  537 
contusion,  535 


Peripheral  nerves  {continued) — 
wounds  of  [continued)  — 
division  complete,  531 

partial,  533 
frequency  in   different   nerves, 

531 
inflammation,  539 
rupture,  538 
Peripheral      neuritis.        See     Neuritis, 

multiple 
Peritonitis,  203,  369 
Permanganate  test  for  meningitis,  436 
Peroneal  muscular  atrophy,  236-237 
Personality,  alternating,  382,  401-402 
"Petit-mal,"  77-78.  267 
Petrous  ganglion  (diagram),  152 
Pharyngeal  reflex,  331 
Pharynx — 

innervation,  172;  paralysis,  172 
Phlebogenic  sciatica,  194 
Phobia?,  383 
Phrenic  neuralgia,  190 
Pill-rolling  tremor,  302 
Pineal  body — • 

anatomy  and  physiology,  32  33 

pathology  of.  33,  475 

precocious  puberty  with  tumours  of, 

33.  475 
tumours  of,  475 
Pituitary  body — 

anatomy  and  physiology,  31-32 
enlargement  in  pregnancy,  32 
lesions  of,  32 

acromegaly  with,  32 
Frbhlich's  syndrome  with.  476 
super  metabolism  in,  32 
tumours  of,  132,  306-307,  453,  476- 
478 
and  hemianopia,  132 
"  Planchette, "  sub-conscious  phenomena 

of,  402 
Plantar  reflex,  2,  35.  222,  230,  332 
Babinski's  phenomenon,  333-334 
in  hysteria,  336,  410 
Pleasure  and  pain,  centres  for,  20,  205 
Pleurodynia,  189 
Plexiform  neuroma,  316 
Plexuses^ 

brachial,  lesions  of,  362. 363, 544-551 
symptoms  in   division  of  pos- 
terior roots,  271 


INDEX 


581 


Plexuses  {continiied)  — 
cervical,  37 
liiinbosaoial,  38 

wounds  of,  554,  555 
solar,    disorders    associated     with, 
346  347 
Pneumonia,  loss  of  deep  reflexes  in,  342 
Pointing  tests,  Barany's,  24,  272 
"  Polar  reactions  "  of  muscle,  422-423 
Polio-encephalitis,  superior,  82 

inferior,  83 
Polio-myelitis,    acute       .SVe    Infantile 
Spinal  Paralysis 
chronic  anterior,  89,  234,  341 
Poly-resthesia,  204 
Polyopia,  monocular,  400 
Polyuria,  hysterical,  412 
Pons — 

arterial  supply,  49 

cranial  nerves  (diagram),  129 

facial  nerve,  origin  in,  157 

haemorrhage,  67,  137 

lesions  of,  11,  61,  95,  162,  209,  212, 

225 
nuclei,  121,  148 
sensory  fibres,  course  in,  17-19 
tumours  of,  475,  482  (tig.) 
Ponto-cerebellar  angle,  lesions  of,  212 

tumours  in,  481  (fig.) 
Ponto-spinal  tract,  14 
Popliteal  nerve,  external,  paralysis,  282, 

300,   536 
"  Port-wine  stains,"  315 
Post-central    region,    wounds    of,    502, 

503 
Post-diphtheritic  paralysis,  120,  163 
Posterior  columns  of  cord,  lesions,  16-20, 

209,  271,  298,  341,  345 
Posterior  fossa,  tumours  of,  183,  341 
Posterior    nerve     roots.         See    Spinal 

Nerves,  Roots 
Postures,  280-293 
cerebellar,  300 
erect  and  at  rest,  280 
in  functional  disease,  287  290 
in  organic  disease,  280,  285-287 
Pot  belly,  252,  300 
Preacher's  hand,  284 
Prc-central  region,  wounds  of,  499-502 
Pre-  and  post  central  region,  wounds  of, 
502-506 


Pregnancy — 

pseudo-,  4 1 1 

tetany  in,  86 
Pressure — 

blood,  in  coma,  63 

intra-cranial,  80,  183.  434,  445-446 
liimliar   puncture   in  relief   of, 
444-445 

intra-thecal,  432-433 

labyrinthine,  171 
Pressure- pain,  14 
Pressure-sense,  199,  202 
Progressive  hypertrophic   neuritis,  237, 

274 
Progressive  muscular  atrophy,  89,   231- 

235,  427 
Progressive  neuritic  amyotrophy  (Char- 
cot and  Marie),  236-237 
"  Pronation    phenomenon  "    in    hemi- 
plegia, 223 
Proptosis,  54,  366 
Protopathic  cutaneous   sensibility,    15  ; 

loss  of,  213  ;  recovery  of,  242 
Pseudo-angina,  190,  410 
Pseudo-appendicitis,  412 
Pseudo-bulbar  paralysis.  123,  226 
Pseudo-hcematemesis,  412 
Pseudo-hnemoptysis,  412 
Pseudo-hypertrophy,  249-252  (figs.) 
Pseudo -pregnancy,  411 
Pseudo-ptosis,  360,  361,  362  ;  hj'sterical, 

146,  407 
Pseudo-sclerosis,  279 
Pseudo-tumor  cerebri,  486 
Psychalgia,  389 
Psychasthenia,  79,  381-383 

imperious  acts  in,  383 

obsessions  in,  382 

phobiffi  of,  383 

stigmata,  381-382 
Psychic  epilepsy,  78 
Psycho-analysis  in  hysteria,  384 
Pterygoid   muscle,    external,    action    in 
congenital  ptosis,  151 

paralysis  of,  154 
Ptosis,  144,  407 

bilateral,  475  -- 

congenital,  150 

hysterical,  144,  146,  407 

pseudo-.     See  above,  Pseudo-ptosig 
Puerperal  eclampsia,  79,  446 


582 


NERVOUS  DISEASES 


Punctured  fractures  of  cranium,  489 
Pupillary  reflex.     See  under  Reflex,  light 
Pupillary  unrest,  138 
Pupils — 

Argyll-Robertson    phenomenon    in, 

136,  139 
contraction — 

in  affections  of  cervical  sympa- 
thetic, 357-367 
in  opium  poisoning,  70 
in  pontine  hpemorrhage,  68 
dilating  fibres,  151,  357  ;  course  of 

(diagi-am),  138 
dilatation  of,  64,  137,  145 
examination  of,  136-140 
inequality  of,  64,  367 
irregularity  in  shape,  137 
Jacksonian  fits  of,  469 
light  reflex.     See  under  Reflexes 
motor  innervation,  136 
painful  stimulation  of  neck  reaction 

to,  140 
paradoxical  reaction,  140 
psychical  dilatation,  140 
reaction  to  accommodation,  139 
size,  variations  in,  136-137 
Pyramidal  cells,  6 
Pyramidal  signs  in  spinal  cord  lesions, 

519 
Pyramidal  tract — 

course,    7,    11,    34  ;    and   diagram 

of,  8 
lesions  of,  7-11 

gait  in,  294-296 

motor   paralysis    due    to.    224- 

226 
reflexes  affected  by,  332-334 


Q. 
QuAPRANTic  hemianopia,  45,  508 
Quinquaud's  sign  of  chronic  alcoholism, 
93 

R. 

Rabies,  84 

"  Raccourcisseurs,      phenomene      des," 

229 
Radial  jerk,  336,  340 
Rami  communicantes,  352 
Raynaud's  disease,  197,  313,  371 


Reactions,  condenser,  425 

of  degeneration,  35,  217,  222,  426 
vou  Recklinghausen's  disease,  316 
Recti  muscles  of  eye,  135,  140-142 
Recurrent  and  transient  motor  paralysis, 

260-268 
Recurrent  lai'yngeal  palsy,  174 
Recurrent  utterances,  114 
Red  nucleus,  connections  (diagram),  12, 
27 

lesions,  95,  149,  279,  475 
Reeling  or  titubating  gait,  270,  299 
Reflected  pains  of  visceral  disease,  190 
Reflex  arc,  2 
Reflex  convulsions,  82 
Reflex  spasms,  102-103 
Reflexes,  330-350 
abdominal,  331 
anal — 

internal,  346,  349 
superficial,  331,  335 
Babiuski's  extensor   plantar  reflex, 

333-334 
Bechterew  and  Mendel's,  344 
Brissaud's,  333 
bulbo-cavernosiis,  331,  335 
carpo-metaearpal,  336 
cilio-spinal,  59,  346,  360 
conditional,  4,  349 
corneal,  75,  159,  331 
cortical  and  spinal,  333 
cremasteric,  331,  335 
ciitaneo-gastric,  346 
dartos,  346,  349 
deep  or  tendon,  336  345 

in  ataxic  conditions,  271 
after  epileptiform  fits,  77,  80 
exaggerated,  21,  342-345 
loss  of,  341-342 

in   upper   and    lower    neurone 
motor  paralyses,  35,  222 
defensive,  229 
effect  of  spinal  injuries  on,  21,  228, 

519,  520-.526 
epigastric,  331 
extensor,  plantar,  333 
flexor,  plantar,  332 
genital,  4,  346 
gluteal,  331 

in  hysteria,  77,  409-410 
jaw,  336 


INDEX 


683 


Reflexes  {continued) — 

light,  2,  137-139,  345 
ill  hysteria,  77,  410 
loss  of,  139 

path  of,  136;  diagrani,  138 
"mark-time,"  229 
oculo-cardiac,  346 
of  non-striated  muscles,  346 
of  sjiinal  automatism,  229 
in  opium  poisoning,  70 
Oppenheim's,  334 
palatal,  331 
paradoxical  flexor,  334 
pharyngeal,  331 
plantar,  2,  35,  64,  70,  222,230,331- 

334 
pronator,  336,  340 
pupillary,  137-140 

mode  of  testing,  138 
radial,  336,  340;  "inversion"   of, 

340 
rectal,  346 
scapular,  331 
scapulohumeral,  336 
scrotal,  346,  349 
sexual,  4,  346 
of  spinal  automatism,  229 
in  spinal  cord  lesions,  520 
superficial  (or  skin),  64,  330-336 
uterine,  346 
vomiting,  4 
Renal  disease.     See  under  Kidney  and 

Nephritis 
Restiforra  body,  25-26,  47 
Retina,  45,  134-135 
Retina   ojdema,  diagnostic   significance, 

66 
Retinitis  pigmentosa,  130 
Retro-bulbar  neuritis,  135 
Retrograde  amnesia,  62 
Retro -quadrigeminal    hemianopia,    light 

reflex  in,  139 
Rheumatic   myositis  of  external  ocular 

muscles,  147 
Rickets,  convulsions  and  tetany  due  to, 

82,  85 
Righthandedness,  46,  47 
Rigidity,  decerebrate,  98 
Rigors,  88 

Rinne's  test  for  hearing,  165 
Risus  sardonicus,  530 


Rolando,  fissure  of,  4,  7,  20 
Romberg's  sign  in  tabes,  270,  271 
Root-areas,  diagrams  of,  43 

posterior,  40 

development  of,  43 
Root-lesions,  203,  233,  245 
Root-pains,  188-189,  196 
Rosenbach's  sign  of  hemiijlegia,  64 
Rossolimo's  toe  phenomenon,  344 
Rotatory   movements,  cerebellar  lesions 
and,  30 

in  intra-cerebellar  growths,  479 
Round-worms,  con\'ulsions  due  to,  82 
Rubro-spinal  tract,  12,  95,  149,  279 

loss  of  function,  341,  475 
Rupophobia,  383 


S. 

Sachal  pain,  192 

Sacral  plexus,  38 

Sacral  segments,  lesions,  335 

Sacro- coccygeal     root  areas     (diagi-am), 

42 
Saliva,  irregularity  in  flow  of,  160 
Saltatory  spasms,  105 
Scapular  reflex,  331 
Scapulo-humeral  reflex,  336 
Sciatic  nerve,  paralysis  of,  241,  242 
Sciatica,  194 

varicose  orphlebogenic,  194 
Scissor  gait,  296 
Scleroderma,  314 
Sclerosis — 

amyotrophic  lateral,   89,  231,  235, 
341 

disseminated.  .    See    Disseminated 
Sclerosis 

multiplex  dolorosa,  189 

postero-lateral,  299 

primary  lateral,  231 

tuberose,  484 
Sclerotomes,  38 

Scotomata,    central,    131,    135;    of  mi- 
graine, 131,  186;   for  red  and  green  in 
tobacco  amblyopia,  131 
Scrotal  reflex,  346,  349 
Sea-sickness,  357 

"  Seelenlahmung,"  Nothnagel's,  407 
Segmental  signs,  in  spinal  cord  lesions, 
518,  519 


584 


NERVOUS  DISEASES 


Segmentation  of  spinal  cord  (diagrams), 

40-43 
Semicircular  canals,  disease  of,  170 
Senile  tremor,  93 
Sensation — 

clinical  investigation  of,  199-203 

paths  of,  16-20 

return  after  mixed  nerve  paralysis, 
242 
Senses,  special,  paths  of,  44-47 
Sensibility,  kinds  of,  14-16 
Sensory  fibres,  position  of,  7-9 

fits,  81 

paths,  16-20 
Serratus  magnus,  paralysis  of,  242 
Sexual  reflex,  4,  346 
Shell  amblyopia,  399 
Shivering,  88 
Shoemakers'  tetany,  86 
Side-gait  ("  Flankengang"),  297 
Sight.     See  Vision 
Sinus,  cavernous,  thrombosis  of,  54 

lateral,  thrombosis,  54,  485 

superior    longitudinal,    thrombosis 
of,  52 
Skew  deviation  of  eyes,  148,  480 
Skin— 

areas  of  peripheral  nerves,  39 

hysterical  affections,  412-413 

pigmentary  changes,  314-318,  369 

sensibility  of,  14-16,  199-202 
loss  of,  213 
recovery  of,  242 

trophic  changes,  309-320 
Sleep,  disorders  of.  451-461 

pathological,  455-456 

physiology  of,  451-455 
Sleeping  sickness,  456 

parasites  in  cerebrospinal  fluid,  439 
Smell,  disorders  of,  81,   128-129,   155; 
hysterical,  391,  397;   olfactory  path, 
44  ;  tests  for  sense  of,  128 
Smile,  spastic,  95 
Sneezing  in  parosmia,  129 
Snellen's  types,  129 
Softening,  cerebral,  traumatic,  496 

spinal,  traumatic,  515 
Somnambulism,  401,  455,  457 
Spasmophilia,  82,  85 
Spasms,  habit,  100 

hysterical,  104,  403,  411 


Spasms  {continued) — 
reflex,  102 
saltatory,  104 
See  cdso  Tics 
Spasmus  nutans,  94 
Spastic  paralysis,  285-287 

extended  type,  286,  345 
flexed  type,  286,  345 
Spastic  smile  or  laugh,  95 
Spasticity,  35,  222,  230-231 
Special  senses,  paths  of,  44-47 
Speech — 

articulation  distinguished  from,  119 
auditory  origin  of,  108 
cortical  centres  for,  107-111 
hysterical  aff'ections,  388 
loss  of — 

aphasia.     See  that  title 
articulation,  defects.    See  Arti- 
culation 
causes,  classification  of,  106 
Sphincter  ani,  externus,  41,  331,  335; 

internus,  346,  349 
Spina  bifida  occulta,  310,  318 
Spinal  accessory  nerve,  177 
Spinal  antesthesia,  447-450 
after-effects  of,  450 
contra-indications,  450 
Spinal  automatism,  reflexes  of,  229 
Spinal  cord — 

arterial  supply,  52 
cervical  region — 

lesions  in,  135,  189,  218,  226, 

521,  523,  526-527 
muscular  localisation  in,  41 
Clarke's  column,  20 
combined  degeneration  of,  272,  345 
compression,  210,  228,  231 
endogenous  tracts,  20 
lateral  column,  11,  17 
lesions  of — 

anesthesia  in,  209-211 
bladder  trouble  due  to,  348 
complete  and  incomplete,  209- 

210,  227,  519-527 
hemi-section   of,    11,    21,   203, 

210,  226,  523 
posterior  roots  and  columns  of, 

16-20,  271 
in  pyramidal  tract.     See  Pyra- 
midal tract 


INDEX 


585 


Spinal  cord  {contini(ed) — 
lesions  of  {contmned)  — 

rectal  incontinence  from,  340 
root  pains  due  to,  196,  filZ 
symptoms  of,  518-519 
trans-section,  complete  of,  209, 

227,  341-342,  r>19-r.22 
unilateral.    Sec  Hemi-sfction  of 
Inmbo-sacral   region.      Sen   Luinlio- 

sacral  cord 
malignant  growths  in,  228,  231,  440 
paths  of  sensation  in,  16 
posterior  colnmns,  16-20,  203,  271, 

298,  341,  34.5 
relations    with     vertebral    cohunn 

(diagram),  430 
root  irritation  from  diseases  of,  190, 

228 
segments  (diagram),  38-40 
snb-acute   combined    degeneration, 

272, 345 
tracts  of,  11-14,  16-20 
tumours,    intra-   and   extra-medul- 
lary, diagnosis  between,  228,  231  ; 
cerebro-spinal  fluid  in,  434 
vaso-motor  centres,  diseases  of,  372 
wounds  of,  515-528 

complete  and  incomplete,  519- 

527 
diagnosis  of  level,  517-519 
pathological  results  of — 
compression,  516 
hemorrhage,  515 
meningo-myelitis,  516 
necrosis,  515,  522 
oedema,  526-528 
signs  and  symptoms  of — 

motor,     pyramidal,     519  ; 

segmental,  518 
sensory,      intramedullary, 
518  ;  root  signs,  517 
Spinal  nerves — 

anterior  roots,  2,  34 ;  lesions  of,  36- 

41,  232-233 
mixed  motor  and  sensory  paralysis 

due  to,  238-239 
motor  paralysis  due  to,  36-41 
posterior  roots — 

cutaneous  areas,  42-43 
distribution,  40-44 
inflammation  of  ganglia,  311 


Spinal  nerves  {conlinned) — 

posterior  roots  (continued) — 

irritation,  188,  196,  20.'.,  209 
lesions  of,  271,  341 
sensory  path  through,  16 
Spino-mnscular  motor  neurone   lesions. 

Sfc  Motor  Paralyses 
S[)ino-thalaniic  tract,  17 
Squint,  141 

Stammering,  125  ;  hysterical,  389  ;  psy- 
chasthenic, 382 
Stellwag's  sign  of  exojihthalmic   goitre, 

366 
Stereognostic  perception,  203,  472 
Sterno-mastoid,  paralysis  of,  175,  177 
Stokes-Adams'  syndrome,  71,  83 
Stomach — 

dilatation  of,  86,  174,  369 

hysterical  rumblings  in,  411 

reflected  pains  of,  191 

reflex  contraction  of,  846 
Stovaine  as  anaesthetic,  447 
StrumpcU's  tibialis  phenomenon,  223 
Strychnine  poisoning,  84,  342,  447,  531 
Stupor,  62 

Sub-cortical  cerebral  tumours,  82 
Sub-cortico  spinal  tracts,  12-14 
Subdural  hremorrhage,  chronic,  66-67 
Sub-pinealisni,  33 
Sub-pituitarism,  307,  476-478 
Sub-thalamic      hemianfesthesia.         See 

HemiauEesthesia 
Subtrapesial  plexus,  paralysis  of,  538 
Sunstroke  and  coma,  72,  185 

treatment  of,  446 
Super-pinealism,   33 
Super-pituitarism,  306-476 
Supinator  jei'k,  340 
Supinator  longus,  paralysis  of,  37 
Sweating — 

abnormalities,  due  to  nerve  disorder, 
364-365,  375-377 

centre,  375-377 

cervical  sympathetic  connected  with, 
357,  360,  361,  364-365 

of  hysteria,  412 

in  Meniere's  disease,  170 

in  spinal  cord  lesions,  376 
Sylvian  fissure,  4,   50,  107  ;  arteries  of, 

50  ;  landmarks  of,  4 
Symmetrical  gangrene,  371 


586 


NERA^OUS  DISEASES 


Sympathetic  nervous  system — 
anatomy  of,  1,  351 
lesions  of,  359,  368 
relation     to     drugs    and     ductless 

glands,  356 
thoracico-abdominal,     diseases    of, 
368 
Sympathetico-tonus,  357 
Syncope  distinguished  from  "  petit-mal," 

78 
Synkinesia,  98,  99,  222,  223 
as  family  stigma,  99 
in  chronic  hemiplegia,  98 
phsyiological,  in  children,  99 
Syphilis — 

cerebro-spinal  fluid  in  diagnosis  of 

lesions,  437,  442-443 
diagnosis  of,  483 
epilepsy  secondary  to,  79 
irregularity    of    pupils    in,     79-80, 

137 
meningitis  of,  188 
palatal  perforation  from,  120 
Third  nerve  palsy  from  (fig.),  145 
Syringobulbia,  211 
Syringomyelia — 

arthropathy   (diagrams),   211,    231, 

324,  328 
claw-hand  in,  284 
dissociated    anaesthesia,    204,    211, 

231 
fibrillary  tremors,  89 
loss  of  deep  reflexes  in,  341 
muscular  wasting  in,  211,  235 
ocular  symptoms,  137 
pain  from,  181 
perforating  ulcers  in,  310 
spontaneous  fractures  in,  324 
thermo-ansestliesia     and    analgesia, 

(diagrams),  210-211,  325 
trophic  changes  in  joints,  231,  323- 
325 

T. 

Tabes — 

anaesthesia   of,    212-213 ;    diagram, 

212 
ankle-jerks,  339 
anosmia,  128 
Argyll -Robertson  phenomenon,  136, 

139 


Tabes  {continued) — 

arthropathy,     diagnosis    of    cases, 
323-325 

ataxia,  270-271 

bulbo-cavcrnosus  reflex,  loss  in,  335 

cerebro-spinal  fluid  in  diagnosis  of, 
442-443 

crises  in,  192,  369 

delayed  sensation  in,  201 

gait  in,  298 

girdle  pains  in,  189 

hypersesthetic  areas,  195,  205  ;  dia- 
gram, 212 

hypotonia  in,  290-291 

involuntary  movements,  99,  323  (fig). 

joint  and   kinaesthetic  senses,    loss 
of,  202 

laryngeal,  122 

lightning  pains,  195,  205 

light  reflex,  loss  of,  139,  345 

muscular  and   tendinous  analgesia, 
203,  212 

myosis,  137 

nasal  crisis,  129 

optic  atrophy,  primary,  135 

perforating  ulcers,  309 

pupils,  irregularity  of,  137 

reflexes,  139,  335,  341,  345 

skin  traction  sense,  loss  of,  201 

spontaneous  fractures,  323 

sudden  falling  in,  267 

trophic  changes,  309,  323-325 

vibration  sense,  loss  of,  203 
Tactile  sense,  14-16,  19-20 

loss  of,  22,  206 
Talipes  equino-varus,  237 
Tangential  wounds  of  head,  489 
Taste,  cortical  centre  for,  47 

course   of    fibres    serving,    47,    152, 
164,  172  ;  diagrams,  152,  161 

disorders  of,  152-153,  160,  164,  172; 
hysterical,  391,  397,  399 

in  Fifth  nerve  palsy,  152 

tests  for  sense  of,  153 
Tear  secretion,  paralysis  of,  155 
Tecto-spinal  tract,  14 
Tegmental  lesions,  95,  475 
Temperature  in  cerebral  hemorrhage,  64 
Temperature   sense,   fibres   serving,   17, 
18,  21 

tests  for,  200 


INDEX 


587 


TemjKJial   lobe,  diseaso   of,  47,   48,   81, 

470,  485 
Temporal  region,  wounds  ul',  509,  510 
Tetanus,  84,  446,  529-531 
Tetany,  84-86,  267 

and  cataract,  86 

Clivostek's  sign  of,  85,  86 

endemic,  of  shoemakers,  86 

Erb's  sign  of,  85 

from  extirpation  of  parathyroids,  85 

Trousseau's  sign  of,  85 
Thalamic  syndrome,  20,   182,  204,  208. 
225,  473-474 

pleasure  and  paiu  in,  205 
Tlialamocortical  pathway,  7 
Thecal  puncture,  i'M 

therapeutic  uses  of  444-450 
Thermic  nystagmus,  143 
Thigh,    motor  points  (Erb's  diagrams), 

420,  422 
Thirst,  cortical  centre  for,  48 
Thomsen's  disease  (Myotonia  congenita), 

262,  425 
Thoracic  nerves,  lesions  producing  ocular 

symptoms,  358 
Thrombosis — 

of  cavernous  sinus,  54 

cerebral,   48,   52-54,    68,   109,   112, 
169,  184,  434 

spinal,  52,  61 
"Tibialis  phenomenon,"  223 
Tic  douloureux,  102,  187 
Tics,  100,  125 

distinguished  from  chorea,  101 

psychasthenic,  382-383 
Tinnitus,  166,  171,  183 
Tobacco  amblyopia,  131,  135 
Tongue — 

ataxy  of,  122 

biting,  in  epilepsy,  76 

hemi-atrophy,  156,  179 

innervation,  152,  172,  178 

paralysis,  120,  178-180 

taste  fibres  to,  152,  160,  172 
Tonic  innervation,  223 

rigidity,  14 
Torcular  Herophili,  52 
Torticollis,    fixed    or    congenital,    280 ; 
labyrinthine.  102;  neuralgic,  102  ;  pro- 
fessional, 102  ;  spasmodic,  101 
Touch.     iSco  Tactile  sense 


Toxicophobia,  383 
Trance,  liysterical,  73,  401 

from  shell-shock,  73 
Traumatic  cerebral  compression,  65,  493 
Tremor,  92  96 

in   progressive  tenticular  degenera- 
tion, 95 
intention,  277 

•  iuinquaud's  sign  in  alcoholism,  93 
senile,  93 

toxic,    92 ;    in    tumours   of   frontal 
lobe,  96 
Trench-feet.  301,  374 
Triceps  jerk,  336,  340 
Trichiuiasis,  247 
Trichoamcsthesia,  199 
Trigeminal  nerve.     Sec  Cranial  Nerves 
Trigeminal  neuralgia,  187-188 
Tromner's  finger  iihenomenon,  344 
Tropho-neuroses,  304-329 
bones  and  joints,  321 
generalised  trophic  disorders,  304 
skin  and  its  appendages.  309 
Trousseau's  sign  of  tetany,  85 
Trypanosome  of  sleeping  sickness,  439 
Tubercles  of  choroid,  135 
Tubercula  dolorosa,  197 
Tuberculin,  Calmette's  and  von  Pirquet's 

reactions,  485 
Tuberculous  meningitis,  183,  438,  439, 

441,  444 
Tuberose  sclerosis,  484 
Tumours — 

abdominal  phantom,  411 
diagnosis,    61,    461  ;    pathological, 

483 
iutra-cranial,  81,  134,  169,  183, 185, 
453,  462  et  scq. 
blue-blindness  in,  132,  463 
central  ganglia,  473 
cerebellum,  166,  169,  186,  276, 
299  ;  ataxia  in,  276  ;  attitude 
of  head  with,  299,  480 ;  extra- 
and  intra-cerebellar,  479-480; 
cortical,    479 ;    lateral    lobe, 
479;  middle  lobe,   479;    fits 
due  to,  74,   86,   480;   skew 
deviation  with,  480 
coma  in,  69 
corona  radiata,  473 
corpora  quadrigcmina,  475 


588 


NERVOUS  DISEASES 


Tumours  [continued) — 

iu tra-  crau ial  [continued) — 
corpus  callosum,  474 
crusta  of  crus  cerebri,  476 
and  drowsiness,  456 
epileptic  fits  from,  80,  464 
fourth  ventricle,  483 
frontal   region,    468  ;    anosmia 

in,  469  ;  tremor  of,  96 
giddiness  in,  465 
headache  of,  183,  185,  463 
hemianopia  from,  10,  132 
internal  capsule,  473 
Jacksonian  fits  in,  466,  467-468 
lumbar  puncture  for  inoperable, 

445 
medulla  oblongata,  483 
mental  dulness  in,  464 
of  mid-brain,  136,  453,  475 
modes  of  producing  symptoms, 

462 
motor  cortex,  467-468 
occipital    lobe,     case     of,     10  ; 

region,  472-473 
optic  neuritis,  134,  463-464 
pineal  body,  475 
pituitary,    132,    306-307,    453, 

476-478 
pons,  482 

ponto-cerebellar,  480 
post-central  convolution,  471 
postero-parietal  lobule,  472 
post-frontal,  469 
pre-central  (fig.),  467 
pre-frontal,  469-470 
slowness  of  breathing,  465  ;  of 

pulse,  465 
supra  -  marginal    and    angular 

convolutions,  471 
tegmental    region    of   crus    or 

pons,  475 
temporal  lobe,  470 
vermis,  479 
vomiting  in,  464 
in  war,  512 
pelvic,  195 

of   spinal    cord,    228  :     diff'erential 
diagnosis,  228-229,  434  ;  menin- 
geal, 188,  189,  195,  196 
Tuning-fork  tests  for  hearing,  165 
Typhus  fever,  "coma-vigil  "  of,  72 


U. 

Ulcers  — 

perforating,  309 

rodent,  313-314 
Ulnar  paralysis,  239,  240,  532,  534 
Ulnar  spasm,  103,  104 
Uncinate  gyrus.     See  under  Gyrus 

fits,  81,  471 
Unilateral  bulbar  syndrome,  275 
Unverricht's  family  myoclonus  (diagram), 

90 
Uraemia — 

coma  of,  71,  456 

convulsions,  79,  82,  514 

Jacksonian  fits  in,  82 
Urine — 

in  alcoholic  poisoning,  70 

diabetic,  71 

dribbling  of,  348 

hysterical  incontinence  and   reten- 
tion, 410  ;  suppression,  412 

reflex  incontinence,  348 

retention,  348 

in  ursemiccoma,  71 
Urticaria  scripta,  375,  413  ;  illustrations, 

146,  414 
Uterine  disease,  headache  from,  184 
Uterine  reflex,  346 

V. 

Vagoxonus,  357 
Varicose  sciatica,  l94 
Vascular  causes  of  insomnia,  458 
Vaso-constriction  in  sleep,  451-452 
Vaso-neuroses,  369-377,  410-413 
Vaso- vagal  attacks,  370 
Vegetative  nervous  system,  351-377 
Veins,  intracranial,  52  55 
Ventral  longitudinal  bundle,  14 
Vermis,  23,  29,  30 

tumours  of,  479 
Vertebral  arteries,  48,  52 
Vertigo — 

causes,  167-172 
Vesical  reflex,  346 
Vestibular  ataxia,  272 
Vestibular  nystagmus,  142 
Vestibular  nerve — 

connections  of,  48 

lesions,  148,  164 

tests  for  integrity,  143 


INDEX 


589 


Vestihulo-spiual  tract,  H,  25,  28 

Vibrant  electricity,  415 

Vibration  sense,  14,  22,  198,  203 

Vidian  nerve,  152 

Visceral  disease,  reflected  pains  in,  190 

Visceral  phenomena  of  hysteria,  410-412 

Vision — 

fibres  of,  path  of,  45-47 
field  of — 

concentric     contraction,      i;J2, 
472  ;     in    myasthenia,    21)1 ; 
hysterical,  397-399 
measurement,  131 
hysterical  blindness,  898 -399 
hypjcraesthesia,  391 
Visual  acuity,  tests  for,  129 
Visual  aphasia.  112  113,  115  ;  diagrams, 
107,  109,  113 
centres  for,  46,  113 
cortical  and  sub-cortical,  112-113 
Visual  cortex,  36-39,  45-47,  471 
Visual  fields,  concentric  contraction  of, 

132 
Visual  hallucinations,  81,  473 
Visual  word-centre,  107,  112,  471 
Visuals  and  auditives,  108,  112 
Vocal  word  centre,  107 
V.  Volkmann's  ischfemic  prralysis,  247- 

248 
Vomiting,   4,  162,  164,  168,   169,   170, 
183,  186 
cerebral,  464 
hysterical,  410-412 
reflex,  4 
"Vorbei-zeigen,"  29,  272,  273 

W. 

Walking.     Sec  Gait 
Wallerian  degeneration,  34,  36 
AVar  lesions  (organic),  487-558 
War  neuroses — 

deaf-mutism,  126 

mutism,  73 

trance,  73 
Wassermann  reaction,  436,  483 
Weber's  law,  202 


Weber's  syndrome,  10,  225,  476 
Weber's  test  fur  hearing,  165 
AVerdnig-Hullniann   tyjie  of  progressive 

muscular  atrophy,  236 
Werner's  "  memoria  tecbnica, "  for  false 

images  (diagram),  141 
Wernicke's  hemiopic  pupillary  reaction, 

139,  473 
Wernicke's  zone,  disintegration  of,  115 
Whitlows,  painless,  211,  310 
Willis,  circle  of,  50 
Witches,  302 

Word-blindness.     iScc  Visual  aphasia 
Word-centre — 

auditory,  107;  diagram,  109,  113 

visual,  107,  lOS 

vocal,  107 
Word-deafness.     Sec  Auditory  aphasia 
Word-swallowing,  101 
Wounds,  of  head,  gaps  in  skull,  491 

penetrating,  490 

perforating,  490 

tangential,  489 
Wounds  of  peripheral  nerves,  531-543 
Wounds  of  spinal  cord,  515,  528 
Wrisberg,  nervus   intermedins  of,   157, 

164 
Wrist  reflex,  336 
Writers'  cramp,  265,  278 
AVriting,  motor  centre  for,  108 

X. 

Xanthochromia  of  cerebro-spinal  fluid, 

434 
X  rays  in  neurology,  415 
in  tumours,  465 


Yawning,    automatic    extensor    move- 
ments in,  98 
in  intra-cranial  disease,  465 
Yohimbine  poisoning,  424 

Z. 

Zacharias,  instance  of  motor  aphasia, 
114 


^ 


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T^he_dia^osis  of  nervousdiseases 


